Misc - 丹野　雅也

AMP Deaminase in Mitochondria-Associated ER Membranes Contributes to Reduction of the Threshold for Mitochondrial Permeability Transition in Type 2 Diabetic Hearts

Arata Osanami, Masaya Tanno, Atsushi Kuno, Hidemichi Kouzu, Toshiyuki Yano, Tatsuya Sato, Tetsuji Miura, Toshifumi Ogawa

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  144  2021年11月

研究発表ペーパー・要旨（国際会議）  

　概要を見る

0

糖尿病性心筋症におけるAMPデアミナーゼの役割

丹野 雅也, 長南 新太, 小川 俊史, 神津 英至

BIO Clinica ( (株)北隆館 )  36 ( 8 ) 762 - 767  2021年07月

　概要を見る

糖尿病性心筋症は発症早期には左室拡張機能障害を呈し、HFpEFの主要な原因の一つとなる。HFpEFは左室仕事量の増加により顕性化する。筆者らは肥満2型糖尿病モデルラットを用いて、2型糖尿病心筋においてはAMPデアミナーゼの活性が亢進していることを見出した。AMPDは圧負荷下において、adenine nucleotide pool減少に基づくATPの枯渇だけではなく、キサンチン酸化還元酵素による活性酸素種産生の増幅とそれに伴うミトコンドリア呼吸障害およびATP産生抑制を介して左室機能障害を促進する。これらの成績からAMPDは糖尿病性心筋症における新たな治療標的になり得ると考えられる。(著者抄録)

J-GLOBAL

冠動脈Stenosisにおける危険因子管理と病変分布の関係:BOREAS-CAG登録データの断面解析【JST・京大機械翻訳】|||

高橋遼, 國分宣明, 小山雅之, 岸上直広, 中田潤, 西川諒, 村上直人, 永野伸卓, 丹野雅也, 大西浩文, 橋本暁佳, 土橋和文, 三浦哲嗣

日本循環器学会学術集会(Web) ( (一社)日本循環器学会 )  85回   OJ06 - 3  2021年03月

J-GLOBAL

AMPデアミナーゼを介した心臓分岐鎖アミノ酸代謝の新規調節:糖尿病心筋症に対する可能な治療標的【JST・京大機械翻訳】|||

OGAWA Toshifumi, KOUZU Hidemichi, OSANAMI Arata, TATEKOSHI Yuki, MIZUNO Masashi, KUNO Atsushi, SUGAWARA Hirohito, FUJITA Yugo, INO Shoya, OHWADA Wataru, SATO Tatsuya, YANO Toshiyuki, MONIWA Norihito, TANNO Masaya, MIURA Tetsuji

日本循環器学会学術集会(Web) ( (一社)日本循環器学会 )  85回   OE081 - 3  2021年03月

J-GLOBAL

糖尿病性心筋症の病態・治療の現状とこれから

丹野雅也, 神津英至, 三浦哲嗣

糖尿病学の進歩   55th  2021年

J-GLOBAL

Empagliflozin attenuates acute kidney injury after myocardial infarction in diabetic rats.

Atsushi Kuno, Yukishige Kimura, Masashi Mizuno, Hiroto Oshima, Tatsuya Sato, Norihito Moniwa, Marenao Tanaka, Toshiyuki Yano, Masaya Tanno, Takayuki Miki, Tetsuji Miura

Scientific reports   10 ( 1 ) 7238 - 7238  2020年04月   [ 国際誌 ]

　概要を見る

Acute kidney injury (AKI) predicts poor prognosis in patients with acute myocardial infarction (MI) and diabetes mellitus (DM) is an independent risk factor of AKI. Recent clinical studies have shown the beneficial effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors on cardiovascular and renal outcomes in patients with DM. We recently reported that canagliflozin normalized susceptibility of diabetic rats to AKI after acute MI via β-hydroxybutyrate-mediated suppression of NOX expression. Here we examined whether the same renoprotective effect is shared by empagliflozin. Serum creatinine levels were not changed by MI induced by coronary artery occlusion in LETO, non-diabetic control rats, and OLETF, obese type 2 diabetic rats. However, immunohistochemistry revealed that MI increased renal expression of NGAL and KIM-1, early markers of tubular injury, by 3.2-fold and 2.6-fold, respectively, in OLETF. These increases in injury markers were not observed in LETO. Pretreatment with empagliflozin of OLETF for 2 weeks improved hyperglycemia, increased blood β-hydroxybutyrate level, and suppressed MI-induced expression of NGAL and KIM-1. Empagliflozin suppressed upregulation of NOX2 and NOX4 in the kidney of OLETF. Taken together with the results of our previous study, it was concluded that treatment with the SGLT2 inhibitor protects the diabetic kidney from MI-induced AKI.

DOI PubMed

糖尿病の心臓においてキサンチンオキシドレダクターゼで仲介される代謝的および機能的機能不全はAMPデアミナーゼの上方制御により増幅される

OSANAMI Arata, IGAKI Yusuke, TANNO Masaya, KOUZU Hidemichi, SATO Tatsuya, KUNO Atsushi, MIURA Tetsuji

日本心不全学会学術集会プログラム・抄録集   24th (CD-ROM)  2020年

J-GLOBAL

非虚血性拡張型心筋症における核MLKLリン酸化の臨床的影響

FUJITA Yugo, YANO Toshiyuki, NISHIKAWA Ryo, NAGANO Nobutaka, KAMIYAMA Naoyuki, FUJITO Takefumi, MOCHIZUKI Atsushi, KOYAMA Masayuki, KOUZU Hidemichi, MURANAKA Atsuko, NAGAHARA Daigo, KUNO Atsushi, TANNO Masaya, MIURA Tetsuji

日本心不全学会学術集会プログラム・抄録集   24th (CD-ROM)  2020年

J-GLOBAL

Longitudinal impact of dapagliflozin treatment on ventricular repolarization heterogeneity in patients with type 2 diabetes

Tatsuya Sato, Takayuki Miki, Shinya Furukawa, Bunzo Matsuura, Yoichi Hiasa, Hirofumi Ohnishi, Masaya Tanno, Tetsuji Miura

Journal of Diabetes Investigation   10 ( 6 ) 1593 - 1594  2019年11月

速報，短報，研究ノート等（学術雑誌）  

DOI PubMed

拡張型心筋症においてnecroptosisの内因性阻害因子caspase-8値の低下は左室拡大と関連する(Reduced Level of Caspase-8, an Endogenous Inhibitor of Necroptosis, is Associated with Left Ventricular Enlargement in Dilated Cardiomyopathy)

藤田 雄吾, 矢野 俊之, 永野 伸卓, 神山 直之, 藤戸 健史, 望月 敦史, 小山 雅之, 神津 英至, 村中 敦子, 永原 大五, 丹野 雅也, 三木 隆幸, 三浦 哲嗣

日本循環器学会学術集会抄録集 ( (一社)日本循環器学会 )  83回   OJ19 - 7  2019年03月

2型糖尿病ラットにおけるキサンチンオキシダーゼの阻害は圧力過負荷誘発拡張機能障害を改善する【JST・京大機械翻訳】|||

井垣勇祐, 丹野雅也, 舘越勇輝, 木村幸滋, 佐藤達也, 神津英至, 矢野俊之, 久野篤史, 三木隆幸, 三浦哲嗣

日本循環器学会学術集会(Web) ( (一社)日本循環器学会 )  83回   OJ40 - 9  2019年03月

J-GLOBAL

糖尿病性心筋症における重要なプレーヤーであるAMPデアミナーゼの新規マイクロRNA仲介調節【JST・京大機械翻訳】|||

TANNO Masaya, TATEKOSHI Yuki, KOUZU Hidemichi, KUNO Atsushi, YANO Toshiyuki, MIKI Takayuki, MIURA Tetsuji

日本循環器学会学術集会(Web)   83rd  2019年

J-GLOBAL

非虚血性拡張型心筋症におけるカスパーゼ8とホスホMLKL,壊死調節蛋白質の顕著な発現

FUJITA Yugo, FUJITA Yugo, YANO Toshiyuki, NAGANO Nobutaka, NISHIKAWA Ryo, KAMIYAMA Naoyuki, FUJITO Takefumi, MOCHIZUKI Atsushi, KOYAMA Masayuki, KOUZU Hidemichi, MURANAKA Atsuko, NAGAHARA Daigo, TANNO Masaya, MIKI Takayuki, MIURA Tetsuji

日本心不全学会学術集会プログラム・抄録集   23rd  2019年

J-GLOBAL

心筋細胞のミトコンドリアダイナミクスに及ぼすネクロトーシスシグナル伝達の活性化の影響

YANO Toshiyuki, ONG Sang-Bing, SATO Tatsuya, KOUZU Hidemichi, KUNO Atsushi, TANNO Masaya, MIKI Takayuki, MIURA Tetsuji

日本心血管内分泌代謝学会学術総会プログラム及び抄録集   23rd  2019年

J-GLOBAL

mTORC1阻害はRIP1阻害媒介TFeB活性化を介して壊死症を減弱する【JST・京大機械翻訳】

Abe Koki, Yano Toshiyuki, Tanno Masaya, Miki Takayuki, Kuno Atsushi, Kuno Atsushi, Sato Tatsuya, Sato Tatsuya, Kouzu Hidemichi, Nakata Kei, Ohwada Wataru, Kimura Yukishige, Sugawara Hirohito, Shibata Satoru, Igaki Yusuke, Ino Shoya, Miura Tetsuji

Biochimica et Biophysica Acta   1865 ( 12 )  2019年

J-GLOBAL

糖尿病の外来診療における慢性合併症評価実態の検討

伊野祥哉, 中田圭, 東浦幸村, 佐藤達也, 矢野俊之, 古橋眞人, 丹野雅也, 三木隆幸, 斎藤重幸, 三浦哲嗣

糖尿病(Web)   62 ( Suppl )  2019年

J-GLOBAL

AMPデアミナーゼ:糖尿病性心筋症のための有望な治療標的

TANNO Masaya, TATEKOSHI Yuki, KOUZU Hidemichi, MIURA Tetsuji

日本心不全学会学術集会プログラム・抄録集   22nd  2018年

J-GLOBAL

冠疾患危険因子の管理目標達成率が冠動脈病変に与える影響

中田圭, 村上直人, 青山ちひろ, 鎌田祐介, 能登貴弘, 国分宜明, 丹野雅也, 三木隆幸, 三浦哲嗣

糖尿病(Web)   61 ( Suppl )  2018年

J-GLOBAL

Dysregulation of miR-301b Contributes to Diabetic Cardiomyopathy via Upregulation of AMP Deaminase in the Vicinity of the Sarcoplasmic Reticulum

Yuki Tatekoshi, Masaya Tanno, Takayuki Miki, Atsushi Kuno, Toshiyuki Yano, Wataru Ohwada, Koki Abe, Yusuke Igaki, Yugo Fujita, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  136  2017年11月

研究発表ペーパー・要旨（国際会議）  

　概要を見る

0

Empagliflozin, an SGLT2 inhibitor, improves survival after myocardial infarction in diabetic rats by up-regulating anti-oxidative stress proteins

H. Oshima, M. Mizuno, T. Miki, A. Kuno, K. Nakata, Y. Kimura, T. Yano, M. Tanno, T. Miura

DIABETOLOGIA ( SPRINGER )  60   S32 - S32  2017年09月

研究発表ペーパー・要旨（国際会議）  

An SGLT-2 inhibitor reverses impaired ventricular repolarisation in patients with type 2 diabetes

T. Sato, T. Miki, H. Ohnishi, T. Yamashita, A. Takada, T. Yano, M. Tanno, A. Tsuchida, T. Miura

DIABETOLOGIA ( SPRINGER )  60   S424 - S425  2017年09月

研究発表ペーパー・要旨（国際会議）  

【高齢者の循環器診療の加齢変化の課題-ここが知りたい-】高齢者糖尿病治療における高血圧 高血圧治療ガイドライン2014の活用

大和田 渉, 丹野 雅也

臨床医のための循環器診療 ( (株)学樹書院 )  ( 26 ) 29 - 31  2017年03月

ミトコンドリア複合体IIIタンパク質であるRieskeのトリステトラプロリン媒介調節は,鉄欠乏に対して心臓を保護する

SATO Tatsuya, TANNO Masaya, YANO Toshiyuki, MIKI Takayuki, KUNO Atsushi, KOUZU Hidemichi, ARDEHALI Hossein, MIURA Tetsuji

日本心不全学会学術集会プログラム・抄録集   21st  2017年

J-GLOBAL

急性心不全患者へのバソプレシンV2受容体遮断薬長期投与の効果:BOREAS-ADHFレジストリ研究

長南新太, 丹野雅也, 能登貴弘, 永野伸卓, 神津英至, 村上直人, 西田絢一, 国分宣明, 三浦哲嗣

日本循環器学会北海道地方会(Web)   118th  2017年

J-GLOBAL

多腺性自己免疫症候群3A型に房室ブロックを合併した一例:抗Ro/SS-A抗体との関連

中田圭, 矢野俊之, 大島洸人, 古橋眞人, 丹野雅也, 斎藤重幸, 三木隆幸, 三浦哲嗣

糖尿病(Web)   60 ( Suppl )  2017年

J-GLOBAL

ROS-Induced Mitochondrial Translocation of Phosphatases Cancels Cell-Protective Signals Activated by Phosphorylation of Mitochondrial Protective Kinases

Wataru Ohwada, Masaya Tanno, Toshiyuki Yano, Atsushi Kuno, Takayuki Miki, Satoko Ishikawa, Yuki Tatekoshi, Koki Abe, Kouhei Ohno, Masashi Mizuno, Kei Nakata, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  134  2016年11月

研究発表ペーパー・要旨（国際会議）  

The Role of AMP Deaminase in Diabetic Cardiomyopathy and Its Regulatory Mechanisms: A Potential Novel Therapeutic Target

Masaya Tanno, Hidemichi Kouzu, Yuki Tatekoshi, Tetsuji Miura

JOURNAL OF CARDIAC FAILURE ( CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS )  22 ( 9 ) S161 - S161  2016年09月

研究発表ペーパー・要旨（国際会議）  

DOI

Aberrant mTORC1 Activation in Cardiomyocytes: A Novel Prognostic Marker and Possible Therapeutic Target in Nonischemic Dilated Cardiomyopathy

Toshiyuki Yano, Masayuki Koyama, Daigo Nagahara, Atsushi Mochizuki, Takefumi Fujito, Masaya Tanno, Takayulci Miki, Tetsuji Miura

JOURNAL OF CARDIAC FAILURE ( CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS )  22 ( 9 ) S174 - S174  2016年09月

研究発表ペーパー・要旨（国際会議）  

Restoration of the intra-mitochondrial interplay between protective signals and malate-aspartate shuttle by continuous erythropoietin receptor activation prevents CKD-induced infarct size enlargement

K. Nishizawa, T. Yano, T. Miki, M. Tanno, A. Kuno, T. Tobisawa, M. Ogasawara, S. Muratsubaki, K. Ohno, M. Mizuno, W. Ohwada, S. Ishikawa, T. Miura

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  37   522 - 523  2016年08月

研究発表ペーパー・要旨（国際会議）  

Sequestration of p62 by RIP1 promotes necroptosis through suppression of autophagic flux in cardiomyocytes; a novel cross-talk between autophagy and necroptosis

T. Yano, M. Ogasawara, T. Miki, M. Tanno, A. Kuno, K. Ohno, K. Nishizawa, W. Owada, M. Mizuno, H. Sugawara, Y. Takekoshi, K. Nakata, S. Ishikawa, T. Miura

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  37   307 - 307  2016年08月

研究発表ペーパー・要旨（国際会議）  

Upregulation of AMP deaminase activity in diabetic hearts by decreased interaction with phosphoglucomutase-1 and depletion of fructose 1,6-diphosphate: a novel mechanism for diabetic cardiomyopathy

Y. Tatekoshi, M. Tanno, H. Kouzu, T. Miki, A. Kuno, S. Ishikawa, T. Yano, W. Ohwada, K. Ohno, M. Mizuno, K. Nishizawa, K. Nakata, T. Miura

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  37   1037 - 1038  2016年08月

研究発表ペーパー・要旨（国際会議）  

Excessive ROS production in mitochondria switches off protective mitochondrial kinase signaling

M. Tanno, W. Ohwada, T. Yano, T. Miki, A. Kuno, S. Ishikawa, Y. Tatekoshi, K. Nishizawa, M. Mizuno, T. Miura

CARDIOVASCULAR RESEARCH ( OXFORD UNIV PRESS )  111   S1 - S1  2016年07月

研究発表ペーパー・要旨（国際会議）  

Ischemic conditioning : pre-, post-, and remote-conditioning (特集 わが国の循環器診療pros・cons : 2016)

丹野 雅也, 三浦 哲嗣

循環器内科 = Cardioangiology ( 科学評論社 )  79 ( 6 ) 522 - 527  2016年06月

CiNii

筋小胞体近傍におけるAMPデアミナーゼの活性亢進:糖尿病性心筋症の新たなメカニズム

TATEKOSHI Yuki, TANNO Masaya, KOUZU Hidemichi, YANO Toshiyuki, KUNO Atsushi, ISHIKAWA Satoko, MIKI Takayuki, MIURA Tetsuji

日本心血管内分泌代謝学会学術総会プログラム及び抄録集   20th  2016年

J-GLOBAL

睡眠呼吸障害が血糖変動に与える影響の検討

中田圭, 丹野雅也, 矢野俊之, 小笠原淳, 赤坂憲, 古橋眞人, 三木隆幸, 三浦哲嗣

糖尿病(Web)   59 ( Suppl )  2016年

J-GLOBAL

Intramolecular Inhibition of Ser473 Phosphorylation by Up-regulated Thr308 Phosphorylation in Akt Contributes to Enlargement of Infarct Size by Chronic Renal Failure

Toshiyuki Tobisawa, Toshiyuki Yano, Takayuki Miki, Masaya Tanno, Atushi Kuno, Hidemichi Kouzu, Makoto Ogasawara, Shingo Muratsubaki, Kohei Ohno, Keitaro Nishizawa, Masashi Mizuno, Wataru Ohwada, Satoko Ishikawa, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  132  2015年11月

研究発表ペーパー・要旨（国際会議）  

Regulation of Mitochondrial Functions by Sirtuin Proteins in Heart Failure

Masaya Tanno, Atsushi Kuno, Yoshiyuki Horio, Tetsuji Miura

JOURNAL OF CARDIAC FAILURE ( CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS )  21 ( 10 ) S158 - S159  2015年10月

研究発表ペーパー・要旨（国際会議）  

Enlargement of Infarct Size by CKD is Preventable by Consistent Activation of the Erythropoietin Receptor

Keitaro Nishizawa, Toshiyuki Yano, Takayuki Miki, Masaya Tanno, Atsushi Kuno, Hidemichi Kouzu, Toshiyuki Tobisawa, Tetsuji Miura

JOURNAL OF CARDIAC FAILURE ( CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS )  21 ( 10 ) S180 - S180  2015年10月

研究発表ペーパー・要旨（国際会議）  

Predictors for atrial fibrillation in patients with coronary artery disease: a cross-sectional analysis of BOREAS registry data

N. Kokubu, H. Akasaka, J. Nishida, N. Nagano, N. Murakami, S. Muratsubaki, M. Tanno, A. Hashimoto, T. Miki, T. Miura

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  36   905 - 905  2015年08月

研究発表ペーパー・要旨（国際会議）  

Dysregulation of two phosphorylation sites in Akt, Thr308 and Ser473, upon reperfusion mediates enlargement of myocardial infarct size by chronic renal failure

T. Tobisawa, T. Yano, T. Miki, A. Kuno, M. Tanno, H. Kouzu, M. Ogasawara, S. Muratsubaki, K. Ohno, T. Miura

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  36   170 - 170  2015年08月

研究発表ペーパー・要旨（国際会議）  

Continuous erythropoietin receptor activation reverses increased myocardial susceptibility to ischemia/reperfusion injury in chronic renal failure

K. Nishizawa, T. Yano, T. Miki, M. Tanno, A. Kuno, H. Kouzu, T. Tobisawa, M. Mizuno, H. Sugawara, T. Miura

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  36   378 - 378  2015年08月

研究発表ペーパー・要旨（国際会議）  

老化と心血管疾患(第4回)心疾患発症における長寿遺伝子の役割

丹野 雅也, 三浦 哲嗣

Anti-aging science : 脳心血管抗加齢研究会機関誌 ( メディカルレビュー社 )  7 ( 1 ) 44 - 48  2015年03月

CiNii

Aktの2つのリン酸化部位間の分子内相互作用の調節異常は慢性腎不全による梗塞サイズの肥大に関与する

TOBISAWA Toshiyuki, YANO Toshiyuki, MIKI Takayuki, TANNO Masaya, KUNO Atsushi, KOUZU Hidemichi, OGASAWARA Makoto, MIURA Tetsuji

日本血管生物医学会学術集会プログラム・抄録集   23rd  2015年

J-GLOBAL

多発脳梗塞を契機に診断された,特発性好酸球増加症候群にLoefller心内膜心筋炎を合併した一例

大岩修太郎, 能登貴弘, 瀬野結, 神津英至, 村中敦子, 矢野俊之, 丹野雅也, 三浦哲嗣

日本循環器学会北海道地方会(Web)   114th  2015年

J-GLOBAL

心不全と糖尿病が,睡眠呼吸障害と血糖変動の関連へ与える影響

藤田雄吾, 中田圭, 丹野雅也, 鈴木洋平, 長南新太, 舘越勇輝, 能登貴弘, 瀬野結, 三木隆幸, 三浦哲嗣

日本循環器学会北海道地方会(Web)   114th  2015年

J-GLOBAL

Accumulation of P62 by Dysregulation of Autophagy Induces Rip1-dependent Necroptosis in Cardiomyocytes: a Novel Interplay Between Autophagy and Necroptosis

Makoto Ogasawara, Toshiyuki Yano, Takayuki Miki, Masaya Tanno, Atsushi Kuno, Hidemichi Kouzu, Hiromichi Murase, Toshiyuki Tobisawa, Shingo Muratsubaki, Keitaro Nishizawa, Masashi Mizuno, Satoko Ishikawa, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  130  2014年11月

研究発表ペーパー・要旨（国際会議）  

Disruption of mTORC2 Integrity Underlies Increased Myocardial Susceptibility to Ischemia/reperfusion Injury in Chronic Renal Failure

Toshiyuki Tobisawa, Toshiyuki Yano, Takayuki Miki, Masaya Tanno, Atsushi Kuno, Hidemichi Kouzu, Hiromichi Murase, Makoto Ogasawara, Shingo Muratsubaki, Masashi Mizuno, Keitaro Nishizawa, Satoko Ishikawa, Hideaki Yoshida, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  130  2014年11月

研究発表ペーパー・要旨（国際会議）  

Activation of mTORC1 in Cardiomyocyte is Associated with Fibrosis and Cardiomyocyte Loss in Heart Failure with Reduced Ejection Fraction

Toshiyuki Yano, Shinya Shimoshige, Atsushi Mochizuki, Takefumi Fujito, Atsuko Muranaka, Satoshi Yuda, Masaya Tanno, Takayuki Miki, Akiyoshi Hashimoto, Kazufumi Tsuchihashi, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  130  2014年11月

研究発表ペーパー・要旨（国際会議）  

Clinical Significance of mTORC1 Activation in Cardiomyocytes in Failing Hearts with Reduced Ejection Fraction

Toshiyuki Yano, Shinya Shimoshige, Atsushi Mochizuki, Takefumi Fujito, Atsuko Muranaka, Satoshi Yuda, Masaya Tanno, Takayuki Miki, Akiyoshi Hashimoto, Tetsuji Miura

JOURNAL OF CARDIAC FAILURE ( CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS )  20 ( 10 ) S188 - S188  2014年10月

研究発表ペーパー・要旨（国際会議）  

リバース・リモデリングへの挑戦 リバース・リモデリングの分子標的 基礎から臨床へ

矢野 俊之, 小山 雅之, 望月 敦史, 神津 英至, 村中 敦子, 下重 晋也, 丹野 雅也, 湯田 聡, 橋本 暁佳, 三木 隆幸, 三浦 哲嗣

日本心臓病学会学術集会抄録 ( (一社)日本心臓病学会 )  62回   JS8 - 5  2014年09月

Insufficient ATP supply due to excessive degradation of adenine nucleotides by AMP deaminase underlies afterload-induced diastolic dysfunction in the type 2 diabetic heart

H. Kouzu, T. Miki, M. Tanno, A. Kuno, T. Yano, H. Murase, T. Tobisawa, M. Ogasawara, S. Muratsubaki, T. Miura

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  35   327 - 327  2014年09月

研究発表ペーパー・要旨（国際会議）  

Inhibition of DPP-4 restores myocardial autophagic flux and reduces mortality after myocardial infarction in diabetic rats

H. Murase, A. Kuno, T. Miki, M. Tanno, T. Yano, H. Kouzu, T. Tobisawa, M. Ogasawara, S. Ishikawa, T. Miura

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  35   443 - 444  2014年09月

研究発表ペーパー・要旨（国際会議）  

Mitochondrial translocation of GSK-3beta, a trigger of mitochondrial permeability transition, is mediated by its N-terminal domain and promoted by interaction with VDAC2.

M. Tanno, T. Miura, T. Miki, A. Kuno, S. Ishikawa, T. Yano, H. Kouzu

CARDIOVASCULAR RESEARCH ( OXFORD UNIV PRESS )  103  2014年07月

研究発表ペーパー・要旨（国際会議）  

DOI

DPP4阻害はBcl2-ベクリン1相互作用の低下を介して心筋自己貪食性フラックスを回復させ,糖尿病ラットの心筋梗塞後の生存を改善する

MURASE Hiromichi, KUNO Atsushi, MIKI Takayuki, TANNO Masaya, YANO Toshiyuki, KOUZU Hidemichi, ISHIKAWA Satoko, MIURA Tetsuji

International Society for Heart Research Annual Meeting of the Japanese Section. Program and Abstracts   31st  2014年

J-GLOBAL

心筋細胞におけるRIP1依存性ネクロプトーシスとオートファジーとの新規相互作用

OGASAWARA Makoto, YANO Toshiyuki, MIKI Takayuki, TANNO Masaya, KUNO Atsushi, KOUZU Hidemichi, ISHIKAWA Satoko, MIURA Tetsuji

International Society for Heart Research Annual Meeting of the Japanese Section. Program and Abstracts   31st  2014年

J-GLOBAL

Activation of the Glucagon-Like Peptide-1 Receptor Restores Myocardial Autophagic Flux and Reduces Mortality After Myocardial Infarction in Diabetic Rats

Hiromichi Murase, Atsushi Kuno, Takayuki Miki, Masaya Tanno, Toshiyuki Yano, Hidemichi Kouzu, Toshiyuki Tobisawa, Makoto Ogasawara, Satoko Ishikawa, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  128 ( 22 )  2013年11月

研究発表ペーパー・要旨（国際会議）  

The Role of mTORC2 and Ribosomal Protein S6 in Cardioprotective Signaling

Toshiyuki Yano, Marcella Ferlito, Toshiyuki Tobisawa, Atsushi Ogasawara, Hiromichi Murase, Atsushi Kuno, Masaya Tanno, Takayuki Miki, Charles Steenbergen, Tetsuji Miura

JOURNAL OF CARDIAC FAILURE ( CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS )  19 ( 10 ) S138 - S138  2013年10月

研究発表ペーパー・要旨（国際会議）  

Type 2 diabetes induces ventricular electrical remodeling with a transmural gradient

T. Tobisawa, T. Sato, S. Yuda, T. Miki, M. Tanno, A. Kuno, T. Kobayashi, H. Akasaka, N. Tohse, T. Miura

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  34   926 - 926  2013年08月

研究発表ペーパー・要旨（国際会議）  

Mechanisms Underlying Mitochondrial Translocation Of GSK-3 beta, A Crucial Inducer Of Mitochondrial Permeability Transition: GSK-3 beta Activity, Interaction With VDAC2 And A Mitochondrial Targeting Sequence

Masaya Tanno, Atsushi Kuno, Satoko Ishikawa, Makoto Ogasawara, Toshiyuki Tobisawa, Hiromichi Murase, Tatsuya Sato, Hidemichi Kouzu, Takayuki Miki, Tetsuji Miura

CIRCULATION RESEARCH ( LIPPINCOTT WILLIAMS & WILKINS )  113 ( 4 )  2013年08月

研究発表ペーパー・要旨（国際会議）  

高血圧による動脈硬化促進の機序 (第5土曜特集 動脈硬化のすべて) -- (危険因子)

丹野 雅也, 三浦 哲嗣

医学のあゆみ ( 医歯薬出版 )  245 ( 13 ) 1148 - 1152  2013年06月

CiNii

酸化ストレスによるミトコンドリア透過性遷移に対するニコランジルの効果

須永 大介, 石川 聡子, 神津 英至, 久野 篤史, 丹野 雅也, 三木 隆幸, 三浦 哲嗣

Therapeutic Research ( ライフサイエンス出版(株) )  34 ( 3 ) 296,304 - 299,304  2013年03月

Reversal of metabolic shift in post-infarct-remodelled hearts: possible novel therapeutic approach

Masaya Tanno, Atsushi Kuno

CARDIOVASCULAR RESEARCH ( OXFORD UNIV PRESS )  97 ( 2 ) 195 - 196  2013年02月

その他  

DOI

急激な血糖悪化を契機に偶然発見され、多腺性内分泌腫瘍症1型が疑われた1例

菅原 浩仁, 小笠原 惇, 伊藤 孝仁, 田中 希尚, 古橋 眞人, 下重 晋也, 丹野 雅也, 三浦 哲嗣

糖尿病 ( (一社)日本糖尿病学会 )  56 ( 1 ) 41 - 41  2013年01月

2型糖尿病はKv4.2とKChIP2のダウンレギュレーションを介して過渡的外向K⁺電流の心内膜下-卓越減少を誘発する

SATO Tatsuya, KOBAYASHI Takeshi, KUNO Atsushi, MURASE Hiromichi, ISHIKAWA Satoko, KOUZU Hidemichi, TANNO Masaya, MIKI Takayuki, MIURA Tetsuji, TOHSE Noritsugu

International Society for Heart Research Annual Meeting of the Japanese Section. Program and Abstracts   30th  2013年

J-GLOBAL

アデニンヌクレオチドの過剰分解によるATP供給の不足が2型糖尿病心臓における負荷後誘導拡張機能障害の基礎である

KOUZU Hidemichi, MIKI Takayuki, TANNO Masaya, KUNO Atsushi, YANO Toshiyuki, MURASE Hiromichi, TOBISAWA Toshiyuki, OGASAWARA Makoto, MIURA Etsuji

Journal of Cardiac Failure   19 ( 10 Supplement 1 )  2013年

J-GLOBAL

ミトコンドリアATP感受性K⁺チャンネルの活性化によるmPTP再閉鎖の機構:酸化ストレス後のGSK3β-Rieske相互作用とROS産生の抑制

SUNAGA Daisuke, TANNO Masaya, ISHIKAWA Satoko, KUNO Atsushi, SATO Tatsuya, KOUZU Hidemichi, MIKI Takayuki, MIURA Tetsuji

International Society for Heart Research Annual Meeting of the Japanese Section. Program and Abstracts   30th  2013年

J-GLOBAL

Titin-isoform Shift May Underlie Distinct Ventricular Responses to Pressure and Volume Overloads in Type 2 Diabetic Heart

Hidemichi Kouzu, Atsushi Kuno, Takayuki Miki, Masaya Tanno, Takahito Itoh, Tatsuya Sato, Daisuke Sunaga, Hiromichi Murase, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  126 ( 21 )  2012年11月

研究発表ペーパー・要旨（国際会議）  

Determinants of Plasma BNP Level in Apparently Healthy Subjects: A Cross-sectional Analysis in the Tanno-Sobetsu Study

Hiroshi Akasaka, Hirofumi Ohnishi, Masaya Tanno, Tetsuji Miura

JOURNAL OF CARDIAC FAILURE ( CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS )  18 ( 10 ) S154 - S154  2012年10月

研究発表ペーパー・要旨（国際会議）  

Resveratrol, a SIRT1 activator, prevents cardiomyopathy in dystrophin-deficient mice by down-regulation of p300

A. Kuno, M. Tanno, T. Miki, S. Ishikawa, Y. Horio, T. Miura

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  33   803 - 803  2012年08月

研究発表ペーパー・要旨（国際会議）  

Modified interaction of inorganic phosphate carrier with cyclophilin D underlies impaired response of diabetic heart to cardioprotection

T. Itoh, T. Miki, M. Tanno, A. Kuno, H. Kouzu, T. Sato, D. Sunaga, H. Murase, S. Ishikawa, T. Miura

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  33   109 - 109  2012年08月

研究発表ペーパー・要旨（国際会議）  

Transient Outward K+ Current (I-To) is Reduced Especially in the Suben-docardium via Downregulation of Kv4.2 and KChIP2 Gene Expression in Obese Type2 Diabetic Rat Hearts

Tatsuya Sato, Takeshi Kobayashi, Atsushi Kuno, Takayuki Miki, Masaya Tanno, Tetsuji Miura, Noritsugu Tohse

BIOPHYSICAL JOURNAL ( CELL PRESS )  102 ( 3 ) 339A - 340A  2012年01月

研究発表ペーパー・要旨（国際会議）  

シクロフィリンDと無機リン担体の相互作用の上昇は糖尿病心臓の心筋保護障害の基礎である

ITOH Takahito, MIKI Takayuki, TANNO Masaya, KUNO Atsushi, KOUZU Hidemichi, SATO Tatsuya, SUNAGA Daisuke, MURASE Hiromichi, ISHIKAWA Satoko, MIURA Tetsuji

International Society for Heart Research Annual Meeting of the Japanese Section. Program and Abstracts   29th  2012年

J-GLOBAL

SIRT1 activation by resveratrol ameliorates dystrophic muscle pathology in mdx mice

Yusuke Hori, Atsushi Kuno, Ryusuke Hosoda, Masaya Tanno, Tetsuji Miura, Kazuaki Shimamoto, Yoshiyuki Horio

JOURNAL OF PHARMACOLOGICAL SCIENCES ( JAPANESE PHARMACOLOGICAL SOC )  118   72P - 72P  2012年

研究発表ペーパー・要旨（国際会議）  

UPR In Endoplasmic Reticulum vs. UPR In Mitochondria In Diabetic Myocardium: Which Is Responsible For Deficient Regulation Of Mitochondrial Permeability Transition Pores?

Takahito Itoh, Hidemichi Kouzu, Takayuki Miki, Masaya Tanno, Atsushi Kuno, Tatsuya Sato, Daisuke Sunaga, Satoko Ishikawa, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  124 ( 21 )  2011年11月

研究発表ペーパー・要旨（国際会議）  

Long-Term Treatment with the SIRT1 Activator Resveratrol Ameliorates Cardiomyopathy in Dystrophin-Deficient Mice

Atsushi Kuno, Yusuke Hori, Masaya Tanno, Hidemichi Kouzu, Takahito Itoh, Daisuke Sunaga, Yoshiyuki Horio, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  124 ( 21 )  2011年11月

研究発表ペーパー・要旨（国際会議）  

GSK-3 beta Translocates to Mitochondria by Oxidant Stress in a Kinase Activity-Dependent Manner and Contributes to Lethal ROS Production

Masaya Tanno, Takayuki Miki, Atsushi Kuno, Hidemichi Kouzu, Takahito Itoh, Tatsuya Sato, Satoko Ishikawa, Daisuke Sunaga, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  124 ( 21 )  2011年11月

研究発表ペーパー・要旨（国際会議）  

Treatment with a Sirt1 Activator Resveratrol Prevents Cardiomyopathy in Dystrophin-Deficient Mice

Atsushi Kuno, Yusuke Hori, Tatsuya Sato, Hidemichi Kouzu, Masaya Tanno, Takayuki Miki, Yoshiyuki Horio, Tetsuji Miura

JOURNAL OF CARDIAC FAILURE ( CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS )  17 ( 9 ) S149 - S149  2011年09月

研究発表ペーパー・要旨（国際会議）  

肥満2型糖尿病ラットの心臓における左室収縮能と活動電位の特性

SATO Tatsuya, TAKADA Akifumi, HOTTA Hiroyuki, MIKI Takayuki, TANNO Masaya, KOBAYASHI Takeshi, MAEDA Sachiko, ICHISE Nobutoshi, KUNO Atsushi, KOHZU Hidemichi, ITOH Takahito, SUNAGA Daisuke, ISHIKAWA Satoko, MIURA Tetsuji, TOHSE Noritsugu

Circulation Journal ( (一社)日本循環器学会 )  75 ( Suppl.I ) 3 - 3  2011年03月

J-GLOBAL

ER(小胞体)およびミトコンドリアにおけるUPR(小胞体ストレス応答)増加によるミトコンドリア膜透過性遷移孔の調節不全は糖尿病性心臓の保護喪失要因となる

ITOH Takahito, KOUZU Hidemichi, MIKI Takayuki, TANNO Masaya, KUNO Atsushi, SATO Tatsuya, SUNAGA Daisuke, ISHIKAWA Satoko, MIURA Tetsuji

International Society for Heart Research Annual Meeting of the Japanese Section. Program and Abstracts   28th  2011年

J-GLOBAL

Increased ER Stress is a Fundamental Mechanism for Impairment of Cardioprotective Signaling in Type 2 Diabetes

Hidemichi Kouzu, Takahito Itoh, Takayuki Miki, Masaya Tanno, Toshiyuki Yano, Tatsuya Sato, Akifumi Takada, Daisuke Sunaga, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  122 ( 21 )  2010年11月

研究発表ペーパー・要旨（国際会議）  

Activation of Sirt1 Suppresses Hypertrophic Response of Cardiomyocytes by Inhibition of H3K9 Acetylation via Proteasome-mediated p300 Degradation.

Atsushi Kuno, Masaya Tanno, Satoko Ishikawa, Yoshiyuki Horio, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  122 ( 21 )  2010年11月

研究発表ペーパー・要旨（国際会議）  

Connexin-43 Contributes to Transmission of MitoK(ATP) Channel-Derived Redox Signal to Akt-GSK-3 beta Pathway in Cardiomyocyte Protection Afforded by G-protein Coupled Receptors

Satoko Ishikawa, Atsushi Kuno, Takayuki Miki, Masaya Tanno, Toshiyuki Yano, Hidemichi Kouzu, Tatsuya Sato, Daisuke Sunaga, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  122 ( 21 )  2010年11月

研究発表ペーパー・要旨（国際会議）  

Ventricular Dysfunction and Blunted Response to Adrenergic Stimulation in Obese Type 2 Diabetes Predispose to Fatal Heart Failure After Infarction: Possible Involvement of MicroRNA-1 Down-Regulation

Akifumi Takada, Takayuki Miki, Masaya Tanno, Hiromu Suzuki, Toshiyuki Yano, Atushi Kuno, Takahito Itoh, Tatsuya Sato, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  122 ( 21 )  2010年11月

研究発表ペーパー・要旨（国際会議）  

Apparently Slight Ventricular Dysfunction Predisposes Obese Type 2 Diabetic Rats to High Mortality After Myocardial Infarction

Hidemichi Kouzu, Akifumi Takada, Takayuki Miki, Masaya Tanno, Toshiyuki Yano, Atsushi Kuno, Takahito Itoh, Tatsuya Satoh, Tetsuji Miura

JOURNAL OF CARDIAC FAILURE ( CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS )  16 ( 9 ) S169 - S169  2010年09月

研究発表ペーパー・要旨（国際会議）  

Activation of SIRT1 modifies histone acetylation/methylation and attenuates cardiomyocyte hypertrophy

Atsushi Kuno, Masaya Tanno, Yoshiyuki Horio

JOURNAL OF PHARMACOLOGICAL SCIENCES ( JAPANESE PHARMACOLOGICAL SOC )  112   200P - 200P  2010年

研究発表ペーパー・要旨（国際会議）  

The SIRT1 Activator Resveratrol Suppresses Cardiomyocyte Hypertrophy by Promoting Histone H3 Lys9 Deacetylation and Tri-methylation

Atsushi Kuno, Masaya Tanno, Toshiyuku Yano, Akifumi Takada, Satoko Ishikawa, Tetsuji Miura, Yoshiyuki Horio, Kazuaki Shimamoto

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  120 ( 18 ) S617 - S617  2009年11月

研究発表ペーパー・要旨（国際会議）  

ROS-mediated Dysregulation of Mitochondrial Permeability Transition Pore Underlies Increased Susceptibility of Hypertensive Hypertrophied Hearts to Ischemia/reperfusion Injury

Toshiyuki Yano, Tetsuji Miura, Takayuki Miki, Masaya Tanno, Atsushi Kuno, Takahito Itoh, Akifumi Takada, Tatsuya Satoh, Kazuaki Shimamoto

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  120 ( 18 ) S784 - S784  2009年11月

研究発表ペーパー・要旨（国際会議）  

Enhanced ANT-cyclophilin-D interaction underlies reduced anti-infarct tolerance and loss of protective response to erythropoietin in hypertensive hypertrophied hearts

T. Miki, T. Yano, T. Miura, M. Tanno, K. Shimamoto

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  30   213 - 213  2009年09月

研究発表ペーパー・要旨（国際会議）  

Activation of histone/protein deacetylase SIRT1 by resveratrol induces MnSOD up-regulation via FOXO3a and improves survival of heart failure animals

A. Kuno, M. Tanno, T. Miura, Y. Horio, K. Shimamoto

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  30   421 - 421  2009年09月

研究発表ペーパー・要旨（国際会議）  

Role of GSK-3beta in negative regulation of mitochondrial permeability transition pore by the mitochondrial KATP channel

T. Miura, Y. Terashima, O. Maas, T. Miki, M. Tanno, S. Ishikawa, K. Shimamoto

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  30   212 - 213  2009年09月

研究発表ペーパー・要旨（国際会議）  

OE-010 Distinct Roles of PKC ε and p38MAPK in Preconditioning-induced Modulation of Gap Junction Permeability during Ischemia(OE02,ACS/AMI (Basic) (IHD),Oral Presentation (English),The 73rd Annual Scientific Meeting of The Japanese Circulation Society)

Yano Toshiyuki, Miura Tetsuji, Miki Takayuki, Tanno Masaya, Naitoh Kazuyuki, Hotta Hiroyuki, Terashima Yoshiaki, Ito Takahito, Hongo Tamaki, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  73   176 - 176  2009年03月

CiNii

OE-036 Roles of GSK-3 β in Myocardial Protection Afforded by Activation of the Mitochondrial K_<ATP> Channel(OE06,Myocardial Ischemia-reperfusion (Basic) (IHD),Oral Presentation (English),The 73rd Annual Scientific Meeting of The Japanese Circulation Society)

Terashima Yoshiaki, Miura Tetsuji, Miki Takayuki, Tanno Masaya, Yano Toshiyuki, Hotta Hiroyuki, Ishikawa Satoko, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  73   183 - 183  2009年03月

CiNii

PE-545 Distinct Roles of FOXO Subtypes in SIRT1-mediated Mn-SOD Up-regulation under Oxidative Stress(PE091,Molecular Biology (M),Poster Session (English),The 73rd Annual Scientific Meeting of the Japanese Circulation Society)

Kuno Atsushi, Tanno Masaya, Miura Tetsuji, Horio Yoshiyuki, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  73   537 - 537  2009年03月

CiNii

FRS-044 ROS-mediated Enhancement of ANT-cyclophilin-D Interaction Underlies Reduced Anti-infarct Tolerance and Lost Response of Cardiomyocytes to Pro-survival Signaling in Hypertrophied Hearts(FRS9,Novel Mechanisms of Myocardial Ischemia (IHD),Featured Research Session (English),The 73rd Annual Scientific Meeting of The Japanese Circulation Society)

Yano Toshiyuki, Miura Tetsuji, Miki Takayuki, Tanno Masaya, Terashima Yoshiaki, Ito Takahito, Ishikawa Satoko, Takada Akifumi, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  73   147 - 147  2009年03月

CiNii

DPE-012 Activation of SIRT1, a Histone/Protein Deacetylase, by Resveratrol Up-regulates MnSOD and Suppresses the Progression of Heart Failure(DPE02,Heart Failure, Basic (M),Digital Poster Session (English),The 73rd Annual Scientific Meeting of The Japanese Circulation Society)

Tanno Masaya, Kuno Atsushi, Ishikawa Satoko, Miura Tetsuji, Miki Takayuki, Horio Yoshiyuki, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  73   358 - 359  2009年03月

CiNii

OE-008 Homodimeric Erythropoietin (EPO) Receptor Provokes More Potent and Distinct Cytoprotective Signaling Compared with Heterodimeric EPO-common-β Subunit Receptor in the Heart(OE02,ACS/AMI (Basic) (IHD),Oral Presentation (English),The 73rd Annual Scientific Meeting of The Japanese Circulation Society)

Satoh Takahiro, Miura Tetsuji, Miki Takayuki, Tanno Masaya, Yano Toshiyuki, Hotta Hiroyuki, Hongo Tamaki, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  73   175 - 176  2009年03月

CiNii

Activation of SIRT1 by resveratrol prevents progression of heart failure and improves the survival in cardiomyopathic hamsters by upregulating MnSOD

Atsushi Kuno, Masaya Tanno, Yoshiyuki Horio

JOURNAL OF PHARMACOLOGICAL SCIENCES ( JAPANESE PHARMACOLOGICAL SOC )  109   112P - 112P  2009年

研究発表ペーパー・要旨（国際会議）  

Rasveratrol, an Activator of Protein Deacetylase SIRT1, Suppresses Oxidative Stress-Induced Call Death by Upregulating MnSOD Expression through Transactivation of FOXO3a

Atsushi Kuno, Masaya Tanno, Tetsuji Miura, Yoshiyuki Horio, Kazuaki Shimamoto

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  118 ( 18 ) S391 - S391  2008年10月

研究発表ペーパー・要旨（国際会議）  

Connexin43-dependent And -independent Mechanisms Of Mitochondrial GSK-3 beta Phosphorylation In Protection Of Cardiomyocyte Against Necrosis

Satoko Ishilkawa, Takayuki Miki, Masaya Tanno, Atsushi Kuno, Takahiro Sato, Hiroyuki Hotta, Yoshiaki Terashima, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  118 ( 18 ) S355 - S355  2008年10月

研究発表ペーパー・要旨（国際会議）  

ER Stress Contributes to Dysregulation Of GSK-3 beta-mediated Suppression of Mitochondrial Permeability Transition in Diabetic Hearts

Takayuki Miki, Masaya Tanno, Atsushi Kuno, Toshiyuki Yano, Takahiro Sato, Hiroyuki Hotta, Satoko Ishikawa, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  118 ( 18 ) S290 - S291  2008年10月

研究発表ペーパー・要旨（国際会議）  

Resveratrol activates protein deacetylase SIRT1 and prolongs the survival of heart failure animals by up-regulating MnSOD through transactivation of FOXO3a

Atsushi Kuno, Masaya Tanno, Tetsuji Miura, Yoshiyuki Horio, Kazuaki Shimamoto

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY ( ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD )  45   S19 - S19  2008年10月

研究発表ペーパー・要旨（国際会議）  

DOI

Role of GSK-3 beta modulation in cytoprotective regulation of mitochondrial permeability transition pores by mitochondrial K-ATP channel activation

Yoshiaki Terashima, Tetsuji Miura, Takayuki Miki, Masaya Tanno, Atsushi Kuno, Toshiyuki Yano, Hiroyuki Hotta, Satoko Ishikawa, Kazuaki Shimamoto

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY ( ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD )  45   S22 - S22  2008年10月

研究発表ペーパー・要旨（国際会議）  

DOI

Activation of a Protein Deacetylase, SIRT1, by Resveratrol Suppresses Progression of Heart Failure and Improves Survival by Up-Regulation of Mn-SOD

Masaya Tanno, Atsushi Kuno, Takayuki Miki, Tetsuji Miura, Yoshiyuki Horio, Kazuaki Shimamoto

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  118 ( 18 ) S388 - S388  2008年10月

研究発表ペーパー・要旨（国際会議）  

Jak2-mediated cardioprotective signaling is lost in diabetic hearts by up-regulation of calcineurin and enhanced ER stress by the AT1 receptor

Hiroyuki Hotta, Tetsuji Miura, Takayuki Miki, Masaya Tanno, Toshiyuki Yano, Yoshiaki Terashima, Kazuaki Shimamoto

JOURNAL OF CARDIAC FAILURE ( CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS )  14 ( 7 ) S163 - S163  2008年09月

研究発表ペーパー・要旨（国際会議）  

PE-222 Alteration of Akt-GSK-3β Signaling by ER Stress Underlies Failure of Erythropoietin to Protect Diabetic Hearts(Myocardial ischemia/reperfusion, basic/clinical(03)(IHD),Poster Session(English),The 72nd Annual Scientific Meeting of the Japanese Circulation Society)

Miki Takayuki, Miura Tetsuji, Tanno Masaya, Yano Toshiyuki, Satoh Takahiro, Hotta Hiroyuki, Terashima Yoshiaki, Simamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  72   415 - 416  2008年03月

CiNii

PE-333 Resveratrol, An Activator of Longevity Protein SIRT1, Suppresses Progression of Heart Failure Through SIRT1-mediated Cardiomyocyte Protection Against Oxidant Stress(Heart failure, basic(03)(M),Poster Session(English),The 72nd Annual Scientific Meeting of the Japanese Circulation Society)

Tanno Masaya, Miura Tetsuji, Miki Takayuki, Yano Toshiyuki, Ohhori Katsuhiko, Horio Yoshiyuki, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  72   443 - 443  2008年03月

CiNii

OJ-104 Connexin-43 Contributes to Pro-survival Akt/GSK-3β signaling And Cardimyocyte Protection in a Receptor-specifit Manner(Cell death, apoptosis/necrosis(M),Oral Presentation(Japanese),The 72nd Annual Scientific Meeting of the Japanese Circulation Society)

Ishikawa Satoko, Miura Tetsuji, Ichikawa Yoshihiko, Tanno Masaya, Ohhori Katsuhiko, Miki Takayuki, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  72   314 - 314  2008年03月

CiNii

PJ-005 Impairment of Myocardial Response to Erythropoietin-Induced Protection in Hypertensive Hypertrophied Hearts(Acute myocardial infarction, basic(02)(IHD),Poster Session(Japanese),The 72nd Annual Scientific Meeting of the Japanese Circulation Society)

Yano Toshiyuki, Miura Tetsuji, Miki Takayuki, Tanno Masaya, Satoh Takahiro, Terashima Yoshiaki, Ishikawa Satoko, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  72   511 - 511  2008年03月

CiNii

OE-309 Relationship of the Mitochondrial K_<ATP> Channel and GSK-3β in Enhancement of Myocardial Tolerance against Infarction(Myocardial ischemia/reperfusion, basic/clinical(01)(IHD),Oral Presentation(English),The 72nd Annual Scientific Meeting of the Japanese Circulation Society)

Terashima Yoshiaki, Miura Tetsuji, Miki Takayuki, Tanno Masaya, Yano Toshiyuki, Hotta Hiroyuki, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  72   258 - 258  2008年03月

CiNii

Resveratrol, an activator of longevity protein SIRT1, suppresses progression of heart failure through SIRT1-mediated cardiomyocyte protection against oxidant stress

Atsushi Kuno, Masaya Tanno, Yoshiyuki Horio

JOURNAL OF PHARMACOLOGICAL SCIENCES ( JAPANESE PHARMACOLOGICAL SOC )  106   213P - 213P  2008年

研究発表ペーパー・要旨（国際会議）  

NAD-dependent histone deacetylase SIRT1 modulates neuronal differentiation by its nuclear translocation

Shin Hisahara, Susumu Chiba, Hiroyuki Matsumoto, Masaya Tanno, Shun Shimohama, Makoto Sato, Yoshiyuki Horio

JOURNAL OF PHARMACOLOGICAL SCIENCES ( JAPANESE PHARMACOLOGICAL SOC )  106   114P - 114P  2008年

研究発表ペーパー・要旨（国際会議）  

Suppression of mitochondrial GSK3 beta activity by its Ser9-phosphorylation contributes to cardiomyocyte protection afforded by erythropoietin against oxidative stress-induced apoptosis

Katsuhiko Ohori, Tetsuji Miura, Masaya Tanno, Takayuki Miki, Takahiro Satoh, Yoshiyuki Horio, Kazuaki Shimamoto

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  116 ( 16 ) 116 - 116  2007年10月

研究発表ペーパー・要旨（国際会議）  

Ser517-phosphorylation of SIRT1 is required for its PI3K/Akt-mediated nuclear translocation and cardiomyocyte protection against oxidant stress in failing hearts

Masaya Tanno, Tetsup Miura, Takayuki Miki, Toshiyuki Yano, Yoshiyuki Horio, Kazuaki Shimamoto

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  116 ( 16 ) 168 - 168  2007年10月

研究発表ペーパー・要旨（国際会議）  

Modification of Akt/GSK-3 beta signaling and mitochondrial GSK-3 beta by ER stress underlies failure of erythropoietin to protect diabetic hearts

Takayuki Miki, Masaya Tanno, Toshyuki Yano, Takahiro Satoh, Hiroyuki Hotta, Katsuhiko Ohori, Satoko Ishikawa, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  116 ( 16 ) 164 - 164  2007年10月

研究発表ペーパー・要旨（国際会議）  

Nuclear translocation of SIRT1 by PI3K/Akt-mediated phosphorylation affords cytoprotection against oxidant stress in post-MI failing hearts

M. Tanno, T. Miura, T. Miki, T. Yano, K. Shimamoto, Y. Horio

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  28   280 - 280  2007年09月

研究発表ペーパー・要旨（国際会議）  

Reduction of ER stress restored insulin sensitivity and myocardial response to erythropoietin induced-protection in diabetic rats

T. Miki, T. Miura, M. Tanno, T. Yano, K. Naitoh, M. Nishihara, T. Satoh, K. Shimamoto

EUROPEAN HEART JOURNAL ( OXFORD UNIV PRESS )  28   433 - 433  2007年09月

研究発表ペーパー・要旨（国際会議）  

Erythropoietin inhibits cardiomyocyte apoptosis through inactivation of glycogen synthase kinase 3 beta

Katsuhiko Ohori, Tetsuji Miura, Masaya Tanno, Takayuki Miki, Toshiyuki Yano, Yoshiyuki Horio, Kazuaki Shimamoto

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY ( ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD )  42   S82 - S82  2007年06月

研究発表ペーパー・要旨（国際会議）  

DOI

OE-053 Cardioprotective Signaling Provoked by Erythropoietin is Impaired in Diabetic Myocardium(Acute myocardial infarction, basic-1, The 71st Annual Scientific Meeting of the Japanese Circulation Society)

Miki Takayuki, Miura Tetsuji, Tanno Masaya, Yano Toshiyuki, Naitoh Kazuyuki, Nishihara Masahiro, Ohhori Katsuhiko, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  71   164 - 165  2007年03月

CiNii

OE-126 Modulation of Mitochondrial Permeability Transition Pore Complex in GSK-3β-mediated Cardiomyocyte Protection(Myocardial ischemia/reperfusion, basic/clinical-1, The 71st Annual Scientific Meeting of the Japanese Circulation Society)

Nishihara Masahiro, Miura Tetsuji, Miki Takayuki, Tanno Masaya, Yano Toshiyuki, Naitoh Kazuyuki, Ohhori Katsuhiko, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  71   183 - 183  2007年03月

CiNii

PE-067 Relationships between p38MAPK and PKC in Connexin43-mediated Gap Junction Modulation by Ischemic Preconditioning(Myocardial ischemia/reperfusion, basic/clinical-2, The 71st Annual Scientific Meeting of the Japanese Circulation Society)

Naitoh Kazuyuki, Miura Tetsuji, Miki Takayuki, Yano Toshiyuki, Tanno Masaya, Takahashi Akari, Satoh Takahiro, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  71   341 - 342  2007年03月

CiNii

OE-312 Nuclear Localization of SIRT1, a Novel Mechanism of Cardiomyocyte Protection in Failing Hearts, is Achieved by PI3K/Akt Signaling(Heart failure, basic-1, The 71st Annual Scientific Meeting of the Japanese Circulation Society)

Tanno Masaya, Sakamoto Jun, Miura Tetsuji, Shimamoto Kazuaki, Horio Yoshiyuki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  71   229 - 229  2007年03月

CiNii

PE-443 Role of Glycogen Synthase Kinase-3 β in Cardiomyocyte Protection by Erythropoietin(Heart failure, basic-5, The 71st Annual Scientific Meeting of the Japanese Circulation Society)

Ohori Katsuhiko, Tanno Masaya, Miura Tetsuji, Miki Takayuki, Yano Toshiyuki, Naitoh Kazuyuki, Nishihara Masahiro, Satoh Takahiro, Horio Yoshiyuki, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  71   435 - 435  2007年03月

CiNii

Nuclear translocation of SIRT1 upregulates Mn-SOD and promotes cardiomyocyte survival in failing hearts.

Masaya Tanno, Jun Sakamoto, Tetsuji Miura, Kazuaki Shimamoto, Yoshiyuki Horio

JOURNAL OF PHARMACOLOGICAL SCIENCES ( JAPANESE PHARMACOLOGICAL SOC )  103   62P - 62P  2007年

研究発表ペーパー・要旨（国際会議）  

Transcriptional activation of histone deacetylase SIRT1 by Notch1 signal

Yoshiyuki Horio, Umefumi Iguchi, Takafumi Ninomiya, Haruyuki Tatsumi, Shin Hisahara, Masaya Tanno, Haruo Takemura

JOURNAL OF PHARMACOLOGICAL SCIENCES ( JAPANESE PHARMACOLOGICAL SOC )  103   105P - 105P  2007年

研究発表ペーパー・要旨（国際会議）  

Both gap junction-dependent and -independent mechanisms contribute to myocardial salvage by delta-opioid receptor activation

K. Naitoh, T. Miura, M. Nishihara, T. Yano, T. Miki, M. Tanno, K. Ohori, K. Shimamoto

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY ( ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD )  41 ( 6 ) 1055 - 1056  2006年12月

研究発表ペーパー・要旨（国際会議）  

DOI

GSK-3 beta signaling module in mitochondria leading to myocardial protection against infarction

Masahiro Nishihara, Takayuki Miki, Masaya Tanno, Toshiyuki Yano, Kazuyuki Naitoh, Katsuhiko Ohori, Akari Takahashi, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  114 ( 18 ) 242 - 242  2006年10月

研究発表ペーパー・要旨（国際会議）  

Increased nuclear translocation of SIRT1 and MnSOD up-regulation in failing hearts: A novel mechanism of the cardiomyocyte death suppression

Tanno Masaya, Tetsuji Miura, Jun Sakamoto, Kazuaki Shimamoto, Yoshiyuki Horio

JOURNAL OF CARDIAC FAILURE ( CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS )  12 ( 8 ) S159 - S160  2006年10月

研究発表ペーパー・要旨（国際会議）  

Contribution of gap junction-dependent and -independent mechanisms to myocardial salvage by delta-opioid receptor activation

Kazuyuki Naitoh, Masahiro Nishihara, Toshiyuki Yano, Takayuki Miki, Masaya Tanno, Katsuhiko Ohori, Akari Takahashi, Tetsuji Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  114 ( 18 ) 311 - 311  2006年10月

研究発表ペーパー・要旨（国際会議）  

PJ-046 Predictors of Improvement of Exercise Capacity by Nitrates in Experimental Heart Failure(Heart failure, basic-7 (M) PJ8,Poster Session (Japanese),The 70th Anniversary Annual Scientific Meeting of the Japanese Circulation Society)

Takahashi Akari, Miura Tetsuji, Miki Takayuki, Sakamoto Jun, Tanno Masaya, Kobayashi Hironori, Nishihara Masahiro, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  70   500 - 500  2006年03月

CiNii

OE-026 Activation of ERK and Suppression of Calcineurin are Interacting Mechanisms of Cardioprotection Afforded by δ-opioid Receptor Activation(Myocardial ischemia-reperfusion, basic/clinical-1 (IHD) OE5,Oral Presentation (English),The 70th Anniversary Annual Scientific Meeting of the Japanese Circulation Society)

Ikeda Yoshihiro, Miura Tetsuji, Sakamoto Jun, Tanno Masaya, Yano Toshiyuki, Naitoh Kazuyuki, Satoh Takahiro, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  70   154 - 155  2006年03月

CiNii

PE-115 Activation of ERK Compensates Disrupted PI3K-Akt Signaling in EPO-induced Cardioprotection of Post-infarct Remodeled Hearts(Acute myocardial infarction, basic-3 (IHD) PE20,Poster Session (English),The 70th Anniversary Annual Scientific Meeting of the Japanese Circulation Society)

Miki Takayuki, Miura Tetsuji, Sakamoto Jun, Tanno Masaya, Naitoh Kazuyuki, Nishihara Masahiro, Takahashi Akari, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  70   363 - 364  2006年03月

CiNii

PE-601 Molecular Mechanisms of Nucleo-cytoplasmic Shuttling of SIRT1, a Histone Deacetylase, and Its Pathopysicological Roles in Cardiomyocytes(Molecular biology, myocardium-2 (M) PE106,Poster Session (English),The 70th Anniversary Annual Scientific Meeting of the Japanese Circulation Society)

Tanno Masaya, Sakamoto Jun, Miura Tetsuji, Shimamoto Kazuaki, Horio Yoshiyuki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  70   482 - 483  2006年03月

CiNii

PE-268 Ischemic Preconditioning Modifies Interactions between Connexin43 and Protein Kinases during Myocardial Ischemia(Myocardial ischemia-reperfusion, basic/clinical-4 (IHD) PE45,Poster Session (English),The 70th Anniversary Annual Scientific Meeting of the Japanese Circulation Society)

Naitoh Kazuyuki, Miura Tetsuji, Yano Toshiyuki, Miki Takayuki, Tanno Masaya, Ikeda Yoshihiro, Ohhori Katsuhiko, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  70   400 - 400  2006年03月

CiNii

The functional significance and mechanisms of nucleo-cytoplasmic shuttling of SIRT1 in failing hearts

M Tanno, J Sakamoto, T Miura, K Shimamoto, Y Horio

JOURNAL OF PHARMACOLOGICAL SCIENCES ( JAPANESE PHARMACOLOGICAL SOC )  100   87P - 87P  2006年

研究発表ペーパー・要旨（国際会議）  

Interaction between ERK and PP2B in development of anti-infarct tolerance of the myocardium

Y Ikeda, T Miura, T Miki, M Tanno, T Yano, H Kobayashi, M Nishihara, K Naitoh, K Oohori, K Shimamoto

JOURNAL OF CARDIAC FAILURE ( CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS )  11 ( 9 ) S316 - S316  2005年12月

研究発表ペーパー・要旨（国際会議）  

Response of silent information regulator 2 alpha (Sir2 alpha) to severe heart failure and its mechanism of nucleo-cytoplasmic shuttling

M Tanno, J Sakamoto, T Miura, K Shimamoto, Y Horio

JOURNAL OF CARDIAC FAILURE ( CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS )  11 ( 9 ) S279 - S279  2005年12月

研究発表ペーパー・要旨（国際会議）  

Antimycin A induced cardioprotection is dependent on pre-ischemic p38-MAPK activation but independent of MKK3

AMN Kabir, XB Cao, DA Gorog, M Tanno, R Bassi, M Bellahcene, RA Quinlan, RJ Davis, RA Flavell, MJ Shattock, MS Marber

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY ( ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD )  39 ( 4 ) 709 - 717  2005年10月

　概要を見る

To examine the role of mitogen-activated protein kinase kinase 3 (MKK3) and p38 mitogen-activated protein kinase (p38-MAPK) in the cardioprotection afforded by antimycin A. Langendorff perfused murine hearts exposed to antimycin A or vehicle prior to global ischemia with p38-MAPK and HSP27 phosphorylation examined in the presence and absence of SB203580 or the presence (mkk3(+/+)) and absence (mkk3(-/-)) of MKK3. Infarct size was determined after 30 or 40 min of global ischemia and 2 h reperfusion. p38-MAPK dual phosphorylation in response to antimycin A was attenuated by co-administration of the antioxidant mercaptopropyonyl-glycine but unaffected by the absence of MKK3 or the presence of SB203580 at a concentration that inhibited the downstream phosphorylation of HSP27. Pre-ischemic exposure to antimycin A caused a significant reduction in subsequent infarction (I:R%) compared to vehicle on both the mkk3(-/-) and mkk3(-/-) background (23.7 +/- 2.9 and 22.8 +/- 4.6 compared to 50.7 +/- 4.0 and 49.6 +/- 5.4 P = 0.001, respectively). In C57B16 mice, antimycin A prior to ischemia reduced infarct size compared to vehicle (22.8 +/- 6.1 vs. 48.3 +/- 5.2 P = 0.01, respectively), an effect abolished by coincident SB203580. The cardiac protection initiated by antimycin A is dependent on the activation of p38-MAPK which occurs, at least in part, in response to oxygen-derived free radicals. The mechanism of this protective form of p38-MAPK activation is independent of the upstream kinase MKK3 and does not involve autophosphorylation. (c) 2005 Elsevier Ltd. All rights reserved.

DOI

Effects of ischemic preconditioning on interactions between Connexin43 and protein kinases during myocardial ischemia

K Naito, T Yano, T Miki, J Sakamoto, M Tanno, A Kuno, Y Ikeda, T Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  112 ( 17 ) U284 - U284  2005年10月

研究発表ペーパー・要旨（国際会議）  

Response of silent information regulator 2 alpha (Sir2 alpha) to severe heart failure and its mechanism of nucleo-cytoplasmic shuttling

M Tanno, J Sakamoto, T Miura, K Shimamoto, Y Horio

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  112 ( 17 ) U360 - U360  2005年10月

研究発表ペーパー・要旨（国際会議）  

P38-MAPK mediates the early negative inotropic effect of tumour necrosis factor-alpha (TNF). Evidence of synergy between a direct negative inotropic effect and coronary constriction

M Bellahcene, XB Cao, J Layland, M Tanno, AM Kabir, RS Haworth, AM Shah, M Avkiran, MS Marber

HEART ( B M J PUBLISHING GROUP )  91   A57 - A57  2005年05月

研究発表ペーパー・要旨（国際会議）  

Erythropoietin Affords Additional Infarct Size-limiting Effects to Preconditioning through Activation of PI3K-Akt-GSK3β Pathway(Acute Myocardial Infarction, Basic 2 (IHD), The 69th Annual Scientific Meeting of the Japanese Circulation Society)

Nishihara Masahiro, Miura Tetsuji, Miki Takayuki, Nakamura Yuichi, Kobayashi Hironori, Naitoh Kazuyuki, Tanno Masaya, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  69   373 - 373  2005年03月

CiNii

Activation of δ-Opioid Receptor Suppresses Myocardial Ischemic Injury by ERK Activation during the Early Phase of Ischemia(Acute Myocardial Infarction, Basic 1 (IHD), The 69th Annual Scientific Meeting of the Japanese Circulation Society)

Ikeda Yoshihiro, Miura Tetsuji, Nakamura Yuichi, Yano Toshiyuki, Tanno Masaya, Sakamoto Jun, Miki Takayuki, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  69   451 - 451  2005年03月

CiNii

Erythropoietin Reduces Myocardial Ischemic Injury, but not Reperfusion Injury, Through Activation of the Pl3k/Akt Pathway(Myocardial Ischemia-reperfusion, Basic 1 (IHD), The 69th Annual Scientific Meeting of the Japanese Circulation Society)

Kobayashi Hironori, Miura Tetsuji, Miki Takayuki, Sakamoto Jun, Tanno Masaya, Nakamura Yuichi, Ikeda Yoshihiro, Hishihara Masahiro, Shimamoto Kazuaki

Circulation journal : official journal of the Japanese Circulation Society ( 社団法人日本循環器学会 )  69   158 - 158  2005年03月

CiNii

Sir2 alpha, an NAD-dependent histon deacetylase, is a nucleo-cytoplasmic shuttling protein

M Tanno, J Sakamoto, T Miura, K Shimamoto, Y Horio

JOURNAL OF PHARMACOLOGICAL SCIENCES ( JAPANESE PHARMACOLOGICAL SOC )  97   80P - 80P  2005年

研究発表ペーパー・要旨（国際会議）  

p38-MAPK mediates the early negative inotropic effect of tumor necrosis factor-alpha. Evidence of synergy between a direct negative inotropic effect and coronary constriction

M Bellahcene, XB Cao, J Layland, M Tanno, AM Kabir, RS Haworth, M Avkiran, MS Marber

HEART ( B M J PUBLISHING GROUP )  90 ( 12 )  2004年12月

研究発表ペーパー・要旨（国際会議）  

MAPKAPK-2 and serine phospharylation of HSP25/27 and alpha B-crystallin do not increase myocardial resistance to infarction

DA Gorog, M Tanno, S Fisher, Bin Cao, X, M Bellahcene, AM Kabir, RA Quinlan, K Kato, MS Marber

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  110 ( 17 ) 67 - 67  2004年10月

研究発表ペーパー・要旨（国際会議）  

p38-MAPK mediates the early negative inotropic effect of TNF-alpha in murine hearts. Evidence of synergy between a direct negative inotropic effect and coronary constriction

M Bellahcene, XB Cao, J Layland, M Tanno, DA Gorog, MS Marber

EUROPEAN HEART JOURNAL ( W B SAUNDERS CO LTD )  25   187 - 187  2004年08月

研究発表ペーパー・要旨（国際会議）  

Antimycin A (AA) a mitochondrial free radical generator mediates cardioprotection via p38 mapkinase (p38)

AMN Kabir, XB Cao, DA Gorog, M Tanno, MJ Shattock, MS Marber

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY ( ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD )  37 ( 1 ) 188 - 188  2004年07月

研究発表ペーパー・要旨（国際会議）  

P38-MAPK activation during myocardial ischaemia. slayer or redeemer

MS Marber, M Tanno, D Gorog, M Bellahcene

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY ( ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD )  37 ( 1 ) 353 - 354  2004年07月

研究発表ペーパー・要旨（国際会議）  

MAPKAPK-2 and serine phosphorylation of HSP25/27 and alpha B-crystallin do not increase myocardial resistance to infarction

DA Gorog, M Tanno, SG Fisher, XB Cao, M Bellahcene, K Dighe, AMN Kabir, RA Quinlan, K Kato, M Gaestel, MS Marber

HEART ( B M J PUBLISHING GROUP )  90   A24 - A24  2004年05月

研究発表ペーパー・要旨（国際会議）  

Antimycin a (AA) mediated cardioprotection is independent of MKK3 but requires PKCe activation

AMN Kabir, XB Cao, M Tanno, R Bassi, MJ Shattock, MS Marber

HEART ( B M J PUBLISHING GROUP )  90   A24 - A24  2004年05月

研究発表ペーパー・要旨（国際会議）  

Inhibition of p38 MAPK activity falls to attenuate contractile dysfunction in a mouse model of low-flow ischemia

DA Gorog, M Tanno, XB Cao, M Bellahcene, R Bassi, AMN Kabir, K Dighe, RA Quinlan, MS Marber

CARDIOVASCULAR RESEARCH ( ELSEVIER SCIENCE BV )  61 ( 1 ) 123 - 131  2004年01月

　概要を見る

Objective: The basal activity of p38 MAPK has recently been shown to impair myocardial contractility. This kinase is activated by ischemia and short-term hibernation. We hypothesized that p38 MAPK activation may contribute to the contractile deficit that characterizes low-flow ischemia. Methods: In Langendorff-perfused isolated C57BL/6 mouse hearts, perfusion pressure was reduced from 85 to 15 or 30 mm Hg for 120 min to induce ischemic left ventricular dysfunction. The effect of the p38 MAPK inhibitor SB203580 (1 muM/l) on contractile function and p38 MAPK activation was assessed. Results: Reduction in perfusion pressure to 15 or 30 min Hg was accompanied by stable reductions in coronary flow (83 +/- 2% and 66 +/- 2%, respectively) and developed pressure (84 +/- 2% and 61 +/- 3%), with minimal infarction (15.6 +/- 0.69% and 10.6 +/- 0.98% of LV myocardium, respectively), but marked activation of p38 MAPK (reflected in pHSP27 1092 +/- 326% basal and 996 +/- 301% basal, respectively). The p38 MAPK inhibitor SB203580, present during the last 60 min of reduced pressure perfusion, prevented p38 MAPK activation (pHSP27 281 +/- 92% basal, p = 0.01 and 186 +/- 72% basal, p = 0.01) but, despite the presence of a contractile reserve, had no effect on developed pressure. Similarly, early treatment with SB203580 started 5 min after the onset of reduced flow also failed to attenuate contractile dysfunction. Conclusion: The p38 MAPK activation that accompanies short-term hibernation does not appear to contribute to the contractile deficit. (C) 2003 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.

DOI

Protective role of gap junctions in preconditioning against myocardial infarction

T Miura, Y Ohnuma, A Kuno, M Tanno, Y Ichikawa, Y Nakamura, T Yano, T Miki, J Sakamoto, K Shimamoto

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY ( AMER PHYSIOLOGICAL SOC )  286 ( 1 ) H214 - H221  2004年01月

　概要を見る

The aim of the present study was to examine the hypothesis that acceleration of gap junction (GJ) closure during ischemia contributes to anti-infarct tolerance afforded by preconditioning (PC). First, the effects of PC on GJ communication during ischemia were assessed. Isolated buffer-perfused rabbit hearts were subjected to 5-min global ischemia with or without PC with two cycles of 5-min ischemia/5-min reperfusion or a GJ blocker (2 mM heptanol), and then the tissue excised from the ischemic region was incubated in anoxic buffer containing lucifer yellow (LY; 2.5 mg/ml), a tracer of GJ permeability, for 20 min at 37degreesC. PC and heptanol significantly reduced the area to which LY was transported in the ischemic myocardium by 39% and by 54%, respectively. In the second series of experiments, three GJ blockers (heptanol, 18beta-glycyrrhetinic acid, and 2,3-butanedione monoxime) infused after the onset of ischemia reduced infarct size after 30-min ischemia/2-h reperfusion to an extent equivalent to that in the case of PC. In the third series of experiments, Western blotting for connexin43 (Cx43) showed that PC shortened the time to the onset of ischemia-induced Cx43 dephosphorylation but reduced the extent of Cx43 dephosphorylation during a 30-min period of ischemia. Calphostin C, a protein kinase C (PKC) inhibitor, abolished preservation of phosphorylated Cx43 but not the early onset of Cx43 dephosphorylation after ischemia in the preconditioned myocardium. These results suggest that PC-induced reduction of GJ permeability during ischemia, presumably by PKC-mediated Cx43 phosphorylation, contributes to infarct size limitation.

DOI

Tumor necrosis factor-induced protection of the murine heart is independent of p38-MAPK activation

M Tanno, DA Gorog, M Bellahcene, XB Cao, RA Quinlan, MS Marber

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY ( ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD )  35 ( 12 ) 1523 - 1527  2003年12月

　概要を見る

Brief exposure to tumor necrosis factor (TNF) is known to trigger subsequent cardioprotection. TNF activates multiple downstream signaling cascades including p38-MAPK, a kinase known to initiate ischemic preconditioning. However, it is not known whether this kinase is similarly involved in TNF-induced cardioprotection. In isolated perfused murine hearts, subjected to 30-min global ischemia/2-h reperfusion, infarction/risk volume was significantly reduced by pretreatment with TNF for 15 min at 0.5 ng/ml, but not at 5 or 10 ng/ml, followed by 10-min washout vs. control (% I/R = 31 +/- 3, 46 +/- 5 or 54 +/- 3 vs. 48 +/- 5; P = 0.01, 0.80 and 0.25, respectively). This was in direct contrast to the concentration dependence of myocardial p38-MAPK phosphorylation, as measured by dual phosphorylated p38-MAPK, which was apparent at TNF concentrations of 5 and 10 ng/ml but not at 0.5 ng/ml vs. time-matched control (as % basal 315 25, 422 94 and 97 +/- 25 vs. 95 +/- 10; P < 0.01, 0.01 and =0.86, respectively). However, phosphorylation of p38-MAPK at 10 min of ischemia was similar among groups (as % basal 393 +/- 98, 410 +/- 67 and 369 +/- 49 for time-matched control, 0.5 and 5 ng/ml, respectively). These patterns were also reflected in the phosphorylation of the downstream substrate HSP27. Furthermore, the effects of TNF on infarct size were not affected by SB203580 (1 mumol/l). These findings suggest that the pre-ischemic activation of p38-MAPK by TNF does not contribute to cardioprotection afforded by this agent. (C) 2003 Elsevier Ltd. All rights reserved.

DOI

Diverse mechanisms of myocardial p38 mitogen-activated protein kinase activation - Evidence for MKK-independent activation by a TAB1-associated mechanism contributing to injury during myocardial ischemia

M Tanno, R Bassi, DA Gorog, AT Saurin, J Jiang, RJ Heads, JL Martin, RJ Davis, RA Flavell, MS Marber

CIRCULATION RESEARCH ( LIPPINCOTT WILLIAMS & WILKINS )  93 ( 3 ) 254 - 261  2003年08月

　概要を見る

The ischemic activation of p38alpha mitogen-activated protein kinase ( p38alpha-MAPK) is thought to contribute to myocardial injury. Under other circumstances, activation is through dual phosphorylation by MAPK kinase 3 (MKK3). Therefore, the mkk3(-/-) murine heart should be protected during ischemia. In retrogradely perfused mkk3(-/-) and mkk3(-/-) mouse hearts subjected to 30 minutes of global ischemia and 120 minutes of reperfusion, infarction/risk volume was similar ( 50 +/- 5 versus 51 +/- 4, P = 0.93, respectively), as was intraischemic p38-MAPK phosphorylation ( 10 minutes ischemia as percent basal, 608 +/- 224 versus 384 +/- 104, P = 0.43, respectively). This occurred despite undetectable activation of MKK3/6 in mkk3(-/-) hearts. However, tumor necrosis factor (TNF)-induced p38-MAPK phosphorylation was markedly diminished in mkk3(-/-) vs mkk3(-/-) hearts ( percent basal, 127 +/- 23 versus 540 +/- 267, respectively, P = 0.04), suggesting an MKK-independent activation mechanism by ischemia. Hence, we examined p38-MAPK activation by TAB1-associated autophosphorylation. In wild-type mice and mkk3(-/-) mice, the p38-MAPK catalytic site inhibitor SB203580 ( 1 mumol/L) diminished phosphorylation during ischemia versus control ( 10 minutes ischemia as percent basal, 143 +/- 2 versus 436 +/- 96, P = 0.003, and 122 +/- 25 versus 623 +/- 176, P = 0.05, respectively) and reduced infarction volume (infarction/risk volume, 57 +/- 5 versus 36 +/- 3, P < 0.001, and 50 +/- 5 versus 29 +/- 3, P = 0.003, respectively) but did not alter TNF-induced activation, although in homogenates of ischemic hearts but not TNF-exposed hearts, p38-MAPK was associated with TAB1. Furthermore, adenovirally expressed wild-type and drug-resistant p38α-MAPK, lacking the SB203580 binding site, was phosphorylated when H9c2 myoblasts were subjected to simulated ischemia. However, SB203580 (1 μmol/L) did not prevent the phosphorylation of resistant p38α-MAPK. These findings suggest the ischemic activation of p38-MAPK contributing to myocardial injury is by TAB1-associated autophosphorylation.

DOI

Inhibition of p38 mitogen-activated protein kinase fails to attenuate contractile dysfunction in a mouse model of low-flow ischaemia

DA Gorog, M Tanno, R Bassi, AMN Kabir, MS Marber

EUROPEAN HEART JOURNAL ( W B SAUNDERS CO LTD )  24   717 - 717  2003年08月

研究発表ペーパー・要旨（国際会議）  

Role of the MAP kinase pathway in the acute negative isotropic effect of tumour necrosis factor-alpha

M Bellahcene, M Tanno, DA Gorog, R Bassi, MS Marber

EUROPEAN HEART JOURNAL ( W B SAUNDERS CO LTD )  24   666 - 666  2003年08月

研究発表ペーパー・要旨（国際会議）  

Varying susceptibility to myocardial infarction among C57BL/6 of different genetic background

DA Gorog, M Tanno, AMN Kabir, GS Kanaganayagam, SG Fisher, R Bassi, MS Marber

EUROPEAN HEART JOURNAL ( W B SAUNDERS CO LTD )  24   175 - 175  2003年08月

研究発表ペーパー・要旨（国際会議）  

Varying susceptibility to myocardial infarction among C57BL/6 mice of different genetic background

DA Gorog, M Tanno, AMN Kabir, GS Kanaganayagam, R Bassi, SG Fisher, MS Marber

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY ( ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD )  35 ( 6 ) 705 - 708  2003年06月

　概要を見る

Genetically manipulated mouse lines are invaluable to investigate the effects of a single gene on sensitivity to ischemia. When choosing appropriate controls, we were concerned that intrinsic, strain-independent but colony-dependent differences may influence the susceptibility to ischemia. We, therefore, compared the infarct:risk volume ratio (I:R%) after 30-min global ischemia in Langendorff-perfused hearts from outbred C57BL/6 mice with that in wild-type mice derived from heterozygote x heterozygote crosses of two different in-house C57BL/6 mouse lines with targeted disruption of an MKK3 or MAPKAPK2 allele. Despite similar hemodynamic characteristics, I:R% in outbred C57BL/6 hearts was significantly smaller (40.8 +/- 2.8%) than in C57BL/6 MAPKAPK2 wild types (65.8 +/- 4.5%, P = 0.0003) and significantly larger than in C57BL/6 MKK3 wild types (23.7 +/- 2.9%, P = 0.002). Therefore, inherent colony substrain-dependent differences appear to influence the susceptibility to infarction in response to global ischemia, underscoring the importance of using colony-matched wild-type controls in marine studies of myocardial ischemia. (C) 2003 Elsevier Science Ltd. All rights reserved.

DOI

Interruption of signal transduction between G protein and PKC-epsilon underlies the impaired myocardial response to ischemic preconditioning in postinfarct remodeled hearts

T Miki, T Miura, M Tanno, J Sakamoto, A Kuno, S Genda, T Matsumoto, Y Ichikawa, K Shimamoto

MOLECULAR AND CELLULAR BIOCHEMISTRY ( KLUWER ACADEMIC PUBL )  247 ( 1-2 ) 185 - 193  2003年05月

　概要を見る

We have recently shown that the protective mechanism of ischemic preconditioning ( PC) is impaired in the myocardium that survived infarction and underwent postinfarct ventricular remodeling. In this study, we examined the hypothesis that failure of PC to activate PKC-epsilon underlies the refractoriness of the remodeling heart to PC. Circumflex coronary arteries were ligated in rabbits to induce infarction and subsequent ventricular remodeling, and only sham operations were performed in controls. Hearts were isolated before (i.e. 4 days later) or after (i.e. 2 weeks later) remodeling of the left ventricle and used for isolated buffer-perfused heart experiments. Myocardial infarction was induced in isolated hearts by 30 min global ischemia/2 h reperfusion, and its size was measured by tetrazolium staining. Using separate groups of hearts, tissue biopsies were taken before and after PC, and PKC translocation was assessed by Western blotting. Areas infarcted in vivo by coronary ligation (CL) were excluded from subsequent infarct size/PKC analyses. In the hearts 4 days after CL, PC with 2 cycles of 5 min ischemia/5 min reperfusion induced PKC-epsilon translocation from cytosol to particulate fractions and limited infarct size to 40% of control value. In the hearts remodeled 2 weeks after CL, PC failed to induce PKC-epsilon translocation and infarct size limitation. In this group, PKC activity and hemodynamic responses to adenosine were similar to those in sham-operated controls. When remodeling after CL was prevented by valsartan infusion (10 mg/kg/day), an angiotensin II type 1 (AT(1)) receptor blocker, PC could induce both infarct limitation and PKC-epsilon translocation. The present results suggest that persistent activation of AT(1) receptors during remodeling disturbed the PC signaling between G proteins and PKC-epsilon, which underlies the refractoriness of the remodeled myocardium to PC.

DOI PubMed CiNii

Diverse mechanisms are responsible for myocardial p38-MAPK activation in response to ischemia and tumour necrosis factor

M Tanno, R Bassi, A Saurin, M Marber

HEART ( B M J PUBLISHING GROUP )  89   A14 - A14  2003年05月

研究発表ペーパー・要旨（国際会議）  

Infarct size limitation by nicorandil: Roles of mitochondrial K-ATP channels, sarcolemmal K-ATP channels, and protein kinase C

A Tsuchida, T Miura, M Tanno, J Sakamoto, T Miki, A Kuno, T Matsumoto, Y Ohnuma, Y Ichikawa, K Shimamoto

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY ( ELSEVIER SCIENCE INC )  40 ( 8 ) 1523 - 1530  2002年10月

　概要を見る

OBJECTIVES This study aimed to examine: 1) whether nicorandil protects the ischemic myocardium by activating sarcolemmal adenosine triphosphate (ATP)-sensitive K+ (sarcK(ATP)) channels or the mitochondrial K-ATP (mitoK(ATP)) channels, and 2) whether protein kinase C (PKC) activity is necessary for cardioprotection afforded by nicorandil. BACKGROUND Nicorandil is a hybrid of nitrate and a K-ATP channel opener that activates the sarcK(ATP) and mitoK(ATP) channels. Both of these K-ATP channels are regulated by PKC, and this kinase may be activated by nitric oxide and also by oxygen free radicals (OFR) generated after mitoK(ATP) channel opening. METHODS In isolated rabbit hearts, infarction was induced by 30-min global ischemia/2-h reperfusion with monitoring of the activation recovery interval (ARI), an index of action potential duration. Protein kinase C translocation was assessed by Western blotting. RESULTS Nicorandil did not change ARI before ischemia, but it accelerated ARI shortening after the onset of ischemia and reduced infarct size by 90%. A sarcK(ATP) channel selective blocker, HMR1098, abolished acceleration of ischemia-induced ARI-shortening by nicorandil and eliminated 40% of nicorandil-induced infarct size limitation. A mitoK(ATP) channel selective blocker, 5-hydroxydecanoate, abolished the protection afforded by nicorandil without affecting ARI. Cardioprotection by nicorandil was inhibited neither by an OFR scavenger, N-2-mercaptopropionylglycine nor by a PKC inhibitor, calphostin C, at a dose that was capable of inhibiting PKC-epsilon translocation after preconditioning. CONCLUSIONS Both the sarcK(ATP) and mitoK(ATP) channels are involved in anti-infarct tolerance afforded by nicorandil, but PKC activation induced by nitric oxide or OFR generation, if any, does not play a crucial role. (C) 2002 by the American College of Cardiology Foundation.

DOI

The role of mitochondrial KATP-channels in preconditioning in the Langendorff-perfused mouse heart - trigger or mediator?

AMN Kabir, M Tanno, DA Gorog, MJ Shattock, MS Marber

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY ( BLACKWELL PUBLISHING ASIA )  29 ( 8 ) A87 - A88  2002年08月

研究発表ペーパー・要旨（国際会議）  

Opening of mitochondrial K-ATP channel occurs downstream of PKC-epsilon activation in the mechanism of preconditioning

Y Ohnuma, T Miura, T Miki, M Tanno, A Kuno, A Tsuchida, K Shimamoto

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY ( AMER PHYSIOLOGICAL SOC )  283 ( 1 ) H440 - H447  2002年07月

　概要を見る

We examined whether the mitochondrial ATP-sensitive K channel (K-ATP) is an effector downstream of protein kinase C-epsilon (PKC-epsilon) in the mechanism of preconditioning (PC) in isolated rabbit hearts. PC with two cycles of 5-min ischemia/5-min reperfusion before 30-min global ischemia reduced infarction from 50.3 +/- 6.8% of the left ventricle to 20.3 +/- 3.7%. PC significantly increased PKC-epsilon protein in the particulate fraction from 51 +/- 4% of the total to 60 +/- 4%, whereas no translocation was observed for PKC-delta and PKC-alpha. In mitochondria separated from the other particulate fractions, PC increased the PKC-epsilon level by 50%. Infusion of 5-hydroxydecanoate (5-HD), a mitochondrial K-ATP blocker, after PC abolished the cardioprotection of PC, whereas PKC-epsilon translocation by PC was not interfered with 5-HD. Diazoxide, a mitochondrial K-ATP opener, infused 10 min before ischemia limited infarct size to 5.2 +/- 1.4%, but this agent neither translocated PKC-epsilon by itself nor accelerated PKC-epsilon translocation after ischemia. Together with the results of earlier studies showing mitochondrial K-ATP opening by PKC, the present results suggest that mitochondrial K-ATP-mediated cardioprotection occurs subsequent to PKC-epsilon activation by PC.

DOI

Opening of the mitochondrial K-ATP channel is downstream of protein kinase C-epsilon activation in the cardioprotective mechanism of ischemic preconditioning

Y Ohnuma, T Miki, M Tanno, S Genda, A Kuno, T Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  104 ( 17 ) 16 - 16  2001年10月

研究発表ペーパー・要旨（国際会議）  

Roles of microtubules and actin filaments in the mechanism of ischemic preconditioning

T Miura, T Miki, Y Ohnuma, M Tanno, K Shimamoto

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  104 ( 17 ) 60 - 60  2001年10月

研究発表ペーパー・要旨（国際会議）  

Blockade of gap junction communication during the early period of ischemia protects cardiomyocytes from infarction

M Tanno, A Tsuchida, Y Nishino, T Matsumoto, S Genda, J Sakamoto, T Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  104 ( 17 ) 43 - 43  2001年10月

研究発表ペーパー・要旨（国際会議）  

Failure of adenosine receptors to activate PKC-epsilon is responsible for loss of cardioprotection of preconditioning in the myocardium undergoing post-infarct remodeling

T Miki, T Miura, A Tsuchida, J Sakamoto, M Tanno, A Kuno, Y Nishino, K Shimamoto

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  104 ( 17 ) 209 - 209  2001年10月

研究発表ペーパー・要旨（国際会議）  

Contribution of both the sarcolemmal K-ATP and mitochondrial K-ATP channels to infarct size limitation by K-ATP channel openers: differences from preconditioning in the role of sarcolemmal K-ATP channels

M Tanno, T Miura, A Tsuchida, T Miki, Y Nishino, Y Ohnuma, K Shimamoto

NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY ( SPRINGER-VERLAG )  364 ( 3 ) 226 - 232  2001年09月

DOI PubMed CiNii

Critical timing of mitochondrial K(ATP) channel opening for enhancement of myocardial tolerance against infarction

A Tsuchida, T Miura, T Miki, A Kuno, M Tanno, Y Nozawa, S Genda, T Matsumoto, K Shimamoto

BASIC RESEARCH IN CARDIOLOGY ( SPRINGER HEIDELBERG )  96 ( 5 ) 446 - 453  2001年09月

　概要を見る

Objective The present study was designed to assess the relationship between the timing of a mitoK(ATP) channel opener, diazoxide, and its infarct size-limiting effect. Methods In isolated rabbit hearts, infarction was induced by 30 min of global ischemia and 2 h of reperfusion, and infarct size was determined by tetrazolium staining and expressed as a percentage of the left ventricle (%IS/LV). Diazoxide, a mitoKATP channel selective opener, and/or 5-hydroxydecanoate (5-HD), a mitoK(ATP) channel blocker, were infused before or after the onset of ischemia. When these agents were infused during the ischemic period, they were dissolved in a hypoxic buffer at concentrations 10-fold higher than those in the pre-ischemic period, and the infusion rate was set at 2 % of the pre-ischemic coronary flow. Results in untreated controls, %IS/LV was 53.2 +/- 4.1 (SE). Pretreatment with diazoxide (100 muM) with a 10-min washout period reduced %IS/LV to 7.8 +/- 2.4 and this protection was abolished by co-infusion of 5-HD (50 muM). Pre-ischemic infusion of diazoxide without a washout period reduced %IS/LV to 7.3 +/- 1.4, and infusion of diazoxide from 10 min after the onset of ischemia also limited %IS/LV to 14.9 +/- 4.6. However, diazoxide infusion from 25 min after the onset of ischemia failed to reduce infarct size (%IS/LV = 54.5 +/- 7.2). Furthermore, pretreatment with 5-HD (50 muM) also completely abolished the protection afforded by early post-ischemic diazoxide infusion (%IS/LV = 48.3 +/- 6.5). Neither infusion of 5-HD nor the anoxic vehicle alone during ischemia modified %IS/LV. Conclusion These findings suggest that opening of mitoKATP channels before ischemia and during early ischemia, but not that upon reperfusion, is important for enhancement of myocardial tolerance against infarction.

DOI

Opening of the mitochondrial KATP channel occurs downstream of protein kinase C in the cardioprotective mechanism of ischaemic preconditioning

T Miki, T Miura, Y Ohnuma, M Tanno, A Kuno, T Matsumoto, K Shimamoto

EUROPEAN HEART JOURNAL ( W B SAUNDERS CO LTD )  22   669 - 669  2001年09月

研究発表ペーパー・要旨（国際会議）  

Infarct size limitation by bradykinin receptor activation is mediated by the mitochondrial but not by the sarcolemmal KATP channel

H Kita, T Miura, T Miki, S Genda, M Tanno, T Fukuma, K Shimamoto

CARDIOVASCULAR DRUGS AND THERAPY ( KLUWER ACADEMIC PUBL )  14 ( 5 ) 497 - 502  2000年09月

　概要を見る

Earlier studies have shown that activation of bradykinin B-2 receptor triggers protein kinase C (PKC)-mediated cardioprotective mechanism in ischemic preconditioning (PC). In the present study, we examined whether the effector in this B-2-receptor triggered pathway of PC is the ATP sensitive potassium (K-ATP) channel in the mitochondria (mito-K-ATP channel) or K-ATP channel in the sarcolemma (sarc-K-ATP channel). Isolated rabbit hearts were perfused with modified Krebs-Henseleit buffer in a Langendorff mode, and regional myocardial ischemia was induced by occluding a left coronary artery for 30 min and then reperfusing for 2 hours. Infarct size was determined by triphenyltetrazolium chloride staining and expressed as a percentage of area at risk (% IS/AR). Infusion of bradykinin (500 nmol/L) for 15 min prior to ischemia significantly reduced % IS/AR from 37.4 +/- 2.9 (SE) of the untreated controls to 12.0 +/- 3.3%. This protective effect of bradykinin was completely abolished by coinfusion of 5-hydroxydecanoate (5-HD, 50 mu mol/L), a selective mito-K-ATP channel blocker (% IS/AR = 44.2 +/- 6.4). In contrast, a high dose of HMR1098 (20 mu mol/L), which is a newly developed sarc-K-ATP channel selective blocker with IC50 of 0.6 mu mol/L, failed to modify the infarct size limitation by preischemic infusion of bradykinin (% IS/AR = 11.7 +/- 3.4). Neither 5-HD nor HMR1098 alone modified infarct size (% IS/AR = 37.8 +/- 3.8 and 35.1 +/- 6.2, respectively). These results suggest that opening of the mito-K-ATP channel but not the sarc-K-ATP channel is involved in infarct size limitation by a mechanism triggered by bradykinin B-2 receptor activation.

DOI

Subtypes of ATP-sensitive potassium channels (KATP) affording anti-infarct tolerance in the heart: mitochondrial KATP versus sarcolemmal KATP

M Tanno, T Miura, A Kuno, T Miki, A Tsuchida, K Shimamoto

EUROPEAN HEART JOURNAL ( W B SAUNDERS CO LTD )  21   669 - 669  2000年08月

研究発表ペーパー・要旨（国際会議）  

コロキウムVII-1 Preconditioning効果 : 基礎の立場から

三浦 哲嗣, 土田 哲人, 三木 隆幸, 丹野 雅也, 野沢 幸永, 現田 聡, 島本 和明

Japanese circulation journal ( 社団法人日本循環器学会 )  64   94 - 94  2000年03月

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P268 Bradykinin受容体を介したpreconditioning機構にはmitochondrial K^<ATP> channelsが寄与する

北 宏之, 三浦 哲嗣, 土田 哲人, 三木 隆幸, 福真 隆行, 丹野 雅也, 野沢 幸永, 松本 倫明, 島本 和明

Japanese circulation journal ( 社団法人日本循環器学会 )  64   526 - 526  2000年03月

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Roles of tyrosine kinase and protein kinase C in infarct size limitation by repetitive ischemic preconditioning in the rat

M Tanno, A Tsuchida, Y Nozawa, T Matsumoto, T Hasegawa, T Miura, K Shimamoto

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY ( LIPPINCOTT WILLIAMS & WILKINS )  35 ( 3 ) 345 - 352  2000年03月

　概要を見る

In this study, we examined the possibility that infarct-size limitation by repetitive preconditioning (PC) is achieved by activation of both protein kinase C (PKC) and tyrosine kinase. In addition, we assessed whether such kinase activation is triggered by angiotensin II type 1 (AT(1)) and alpha(1)-adrenergic receptors and whether sarcolemmal and mitochondrial adenosine triphosphate (ATP)-sensitive potassium (K-ATP) channels play roles as effecters of cardioprotection in the rat. Under pentobarbital anesthesia, myocardial infarction was induced by 20-min coronary occlusion and 3-h reperfusion in the rat. Infarct size was determined by tetrazolium and expressed as a percentage of area at risk (%IS/AR). PC with one cycle of 5-min ischemia/5-min reperfusion before 20-min ischemia significantly reduced %IS/AR from the control value of 49.4 +/- 2.0 to 35.4 +/- 2.8, and repetitive PC with two cycles of 5-min ischemia/5-min reperfusion further limited %IS/AR to 3.2 +/- 0.9. Infarct-size limitation by single-cycle PC was completely abolished by a PKC inhibitor, staurosporine (100 mu g/kg; %IS/ AR, 45.7 +/- 5.0). In contrast, the cardioprotection by repetitive PC was only partially blocked by staurosporine (%IS/AR, 19.8 +/- 2.4), another PKC inhibitor, polymyxin B (5 mg/kg; %IS/AR, 16.2 +/- 3.1), or a tyrosine kinase inhibitor, genistein (5 mg/kg; %IS/AR, 21.8 +/- 1.4). However, a combined injection of genistein and staurosporine additively inhibited protection of repetitive PC (%IS/AR, 36.4 +/- 1.7). Staurosporine, polymyxin B, or genistein alone did not modify %IS/AR in nonpreconditioned rat hearts. Infarct-size limitation by repetitive PC was not attenuated by pretreatment with a selective AT(1)-receptor blocker (CV11974, 10 mg/kg), prazosin (0.6 mg/kg; %IS/AR, 6.4 +/- 3.2 and 1.6 +/- 0.5, respectively). A selective blocker of mitochondrial K-ATP channels, 5-hydroxydecanoate (3 mg/kg), completely abolished the cardioprotective effect (%IS/AR, 50.8 +/- 3.5), but HMR1883 (3 mg/kg), a selective blocker of sarcolemmal K-ATP channels, failed to inhibit the preconditioning effect (%IS/AR, 4.4 +/- 0.7). These findings suggest that repetition of PC provokes activation of both PKC and tyrosine kinase, leading to enhanced antiinfarct tolerance by opening of mitochondrial but not sarcolemmal K-ATP channels. It is unlikely that activation of either AT(1) or alpha(1)-adrenergic receptor alone is crucial to trigger preconditioning.

DOI PubMed CiNii

Critical timing of mitochondrial K-ATP channel opening for enhancement of myocardial tolerance against infarction

A Tsuchida, A Kuno, M Tanno, Y Nozawa, T Miura

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  100 ( 18 ) 631 - 631  1999年11月

研究発表ペーパー・要旨（国際会議）  

0389 プレコンディショニングの反復による梗塞抑制効果の増強におけるtyrosine kinaseとprotein kinase Cの関与

丹野 雅也, 土田 哲人, 三浦 哲嗣, 野沢 幸永, 長谷川 徹, 島本 和明

Japanese circulation journal ( 社団法人日本循環器学会 )  63 ( 1 ) 245 - 245  1999年03月

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Both tyrosine kinase and protein kinase C (PKC) are involved in infarct size limitation by repetitive preconditioning (PC) in the rat

M Tanno, A Tsuchida, T Miura, T Hasegawa, K Shimamota

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  98 ( 17 ) 71 - 71  1998年10月

研究発表ペーパー・要旨（国際会議）  

0164 Ischemic preconditioning(PC)におけるATP-sensitive potasium channel(K_<ATP>)の寄与は虚血障害の持続時間に依存する

丹野 雅也, 土田 哲人, 野沢 幸永, 中野 淳, 三浦 哲嗣, 島本 和明

Japanese circulation journal ( 社団法人日本循環器学会 )  61   152 - 152  1997年03月

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