Misc - TATEKOSHI Yuki

Impact of Mitochondrial Dynamics on Necroptosis in Cardiomyocytes(タイトル和訳中)

戸田 悠貴, 矢野 俊之, 久野 篤史, 丹野 雅也, 神津 英至, 佐藤 達也, 大和田 渉, 舘越 勇輝, 小川 俊史, 清水 将輝, 古橋 眞人

日本循環器学会学術集会抄録集 ( (一社)日本循環器学会 )  88回   PJ080 - 3  2024.03

Administration of Nicotinamide Mononucleotide, a Precursor of NAD+, Attenuates Doxorubicin-induced Cardiotoxicity and Renal Tubular Injury in Mice(タイトル和訳中)

齊藤 圭司, 細田 隆介, 嵯峨 幸夏, 舘越 勇輝, 久野 篤史

日本循環器学会学術集会抄録集 ( (一社)日本循環器学会 )  88回   PJ114 - 4  2024.03

DNA damage and nuclear morphological changes in cardiac hypertrophy are mediated by SNRK through actin depolymerization.

Paulina Stanczyk, Yuki Tatekoshi, Jason S Shapiro, Krithika Nayudu, Yihan Chen, Zachary Zilber, Matthew Schipma, Adam De Jesus, Amir Mahmoodzadeh, Ashley Akrami, Hsiang-Chun Chang, Hossein Ardehali

bioRxiv : the preprint server for biology    2023.07  [International journal]

Authorship：   Lead author

Internal/External technical report, pre-print, etc.  

　View Summary

BACKGROUND: Proper nuclear organization is critical for cardiomyocyte (CM) function, as global structural remodeling of nuclear morphology and chromatin structure underpins the development and progression of cardiovascular disease. Previous reports have implicated a role for DNA damage in cardiac hypertrophy, however, the mechanism for this process is not well delineated. AMPK family of proteins regulate metabolism and DNA damage response (DDR). Here, we examine whether a member of this family, SNF1-related kinase (SNRK), which plays a role in cardiac metabolism, is also involved in hypertrophic remodeling through changes in DDR and structural properties of the nucleus. METHODS: We subjected cardiac specific (cs)- Snrk -/- mice to trans-aortic banding (TAC) to assess the effect on cardiac function and DDR. In parallel, we modulated SNRK in vitro and assessed its effects on DDR and nuclear parameters. We also used phospho-proteomics to identify novel proteins that are phosphorylated by SNRK. Finally, co-immunoprecipitation (co-IP) was used to verify Destrin (DSTN) as the binding partner of SNRK that modulates its effects on the nucleus and DDR. RESULTS: cs- Snrk -/- mice display worse cardiac function and cardiac hypertrophy in response to TAC, and an increase in DDR marker pH2AX in their hearts. Additionally, in vitro Snrk knockdown results in increased DNA damage and chromatin compaction, along with alterations in nuclear flatness and 3D volume. Phospho-proteomic studies identified a novel SNRK target, DSTN, a member of F-actin depolymerizing factor (ADF) proteins that directly binds to and depolymerize F-actin. SNRK binds to DSTN, and DSTN downregulation reverses excess DNA damage and changes in nuclear parameters, in addition to cellular hypertrophy, with SNRK knockdown. We also demonstrate that SNRK knockdown promotes excessive actin depolymerization, measured by the increased ratio of globular (G-) actin to F-actin. Finally, Jasplakinolide, a pharmacological stabilizer of F-actin, rescues the increased DNA damage and aberrant nuclear morphology in SNRK downregulated cells. CONCLUSIONS: These results indicate that SNRK is a key player in cardiac hypertrophy and DNA damage through its interaction with DSTN. This interaction fine-tunes actin polymerization to reduce DDR and maintain proper CM nuclear shape and morphology. CLINICAL PERSPECTIVE: What is new? Animal hearts subjected to pressure overload display increased SNF1-related kinase (SNRK) protein expression levels and cardiomyocyte specific SNRK deletion leads to aggravated myocardial hypertrophy and heart failure.We have found that downregulation of SNRK impairs DSTN-mediated actin polymerization, leading to maladaptive changes in nuclear morphology, higher DNA damage response (DDR) and increased hypertrophy. What are the clinical implications? Our results suggest that disruption of DDR through genetic loss of SNRK results in an exaggerated pressure overload-induced cardiomyocyte hypertrophy.Targeting DDR, actin polymerization or SNRK/DSTN interaction represent promising therapeutic targets in pressure overload cardiac hypertrophy.

DOI PubMed

Temporal Trends in Mortality Attributable to Heart Failure between 2005 and 2019: Insights from Japanese Vital Statistics(タイトル和訳中)

田中 仁啓, 舘越 勇輝, 藤本 恒, 夜久 英憲, カーン サディヤ, グリーンランド フィリップ

日本循環器学会学術集会抄録集 ( (一社)日本循環器学会 )  87回   OJ54 - 5  2023.03

SIRT2 inhibition protects against cardiac hypertrophy and heart failure.

Xiaoyan Yang, Hsiang-Chun Chang, Yuki Tatekoshi, Maryam Balibegloo, Rongxue Wu, Chunlei Chen, Tatsuya Sato, Jason Shapiro, Hossein Ardehali

bioRxiv : the preprint server for biology    2023.01  [International journal]

Authorship：   Lead author

Internal/External technical report, pre-print, etc.  

　View Summary

Sirtuins (SIRT) exhibit deacetylation or ADP-ribosyltransferase activity and regulate a wide range of cellular processes in the nucleus, mitochondria and cytoplasm. The role of the only sirtuin that resides in the cytoplasm, SIRT2, in the development of heart failure (HF) and cardiac hypertrophy is not known. In this paper, we show that the hearts of mice with deletion of Sirt2 ( Sirt2 -/- ) display improved cardiac function after ischemia-reperfusion (I/R) and pressure overload (PO), suggesting that SIRT2 exerts maladaptive effects in the heart in response to stress. Similar results were obtained in mice with cardiomyocyte-specific Sirt2 deletion. Mechanistic studies suggest that SIRT2 modulates cellular levels and activity of nuclear factor (erythroid-derived 2)-like 2 (NRF2), which results in reduced expression of antioxidant proteins. Deletion of Nrf2 in the hearts of Sirt2 -/- mice reversed protection after PO. Finally, treatment of mouse hearts with a specific SIRT2 inhibitors reduces cardiac size and attenuates cardiac hypertrophy in response to PO. These data indicate that SIRT2 has detrimental effects in the heart and plays a role in the progression of HF and cardiac hypertrophy, which makes this protein a unique member of the SIRT family. Additionally, our studies provide a novel approach for treatment of cardiac hypertrophy by targeting SIRT2 pharmacologically, providing a novel avenue for the treatment of this disorder.

DOI PubMed

A Novel Mechanism in the Pathogenesis of Heart Failure With Preserved Ejection Fraction Through Hexokinase Mitochondrial Dislocation and Substrate Shuttling Into the O-Glcnacylation Machinery

Yuki Tatekoshi, Jason S. Shapiro, Mingyang Liu, George M. Bianco, Farzaneh Sharifzad, Adam De Jesus, Navid Koleini, Andrew Wasserstrom, Hossein Ardehali

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  146  2022.11

Authorship：   Lead author

Research paper, summary (international conference)  

　View Summary

0

Post-Transcriptional Regulation of Cardiac Fatty Acid Metabolism by the Tandem Zinc Finger Mrna Binding Protein

Mohammad Keykhaei, Hsiang-Chun Chang, Tatsuya Sato, Konrad Sawicki, Jason S. Shapiro, Yuki Tatekoshi, Hossein Ardehali

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  146  2022.11

Research paper, summary (international conference)  

　View Summary

0

Protein O-GlcNAcylation mediated by hexokinase mitochondrial localization underlies the pathogenesis of heart failure with preserved ejection fraction

Yuki Tatekoshi, Jason S. Shapiro, Mingyang Liu, George M. Bianco, Hossein Ardehali

Keystone Symposia: Heart Failure: Mechanisms and Therapies Program   Poster#2015  2022.09

Authorship：   Lead author

Research paper, summary (international conference)  

Dislocation Of Hexokinase1 From Mitochondria Results In Heart Failure With Preserved Ejection Fraction Through Hyper Oglcnacylation In Endothelial Cells.

Yuki Tatekoshi, Jason S. Shapiro, Farnaz K. Nejad, Mingyang Liu, Krithika Nayudu, Chunlei Chen, Hossein Ardehali

CIRCULATION RESEARCH ( LIPPINCOTT WILLIAMS & WILKINS )  131  2022.08

Authorship：   Lead author

Research paper, summary (international conference)  

DOI

AMPデアミナーゼによる心臓分岐鎖アミノ酸代謝の新規制御 糖尿病性心筋症の治療標的としての期待(Novel Regulation of Cardiac Branched-chain Amino Acid Metabolism through AMP Deaminase: A Possible Therapeutic Target for Diabetic Cardiomyopathy)

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抄録集 ( (一社)日本循環器学会 )  85回   OE081 - 3  2021.03

J-GLOBAL

Abnormal Regulation of P53-mTOR Pathway by MRNA-binding Protein ZFP36L2 in Peri-partum Cardiomyopathy

Yuki Tatekoshi, Hidemichi Kouzu, Hsiang-Chun Chang, Jason S. Shapiro, Adam D. Jesus, Warren A. Mcgee, Issam Ben-Sahra, Chunlei Chun, Hossein Ardehali

CIRCULATION ( LIPPINCOTT WILLIAMS & WILKINS )  142  2020.11

Authorship：   Lead author

Research paper, summary (international conference)  

　View Summary

0

Loss of the RNA-binding Protein ZFP36L2 Results in Peri-partum Cardiomyopathy Through Dysregulation of the P53-mTOR Pathway

Yuki Tatekoshi, Hidemichi Kouzu, Jason S. Shapiro, Hsiang-Chun Chang, Adam D. Jesus, Paulina J. Stanczyk, Issam Ben-Sahra, Perry Blackshear, Hossein Ardehali

CIRCULATION RESEARCH ( LIPPINCOTT WILLIAMS & WILKINS )  127  2020.07

Authorship：   Lead author

Research paper, summary (international conference)  

DOI

2型糖尿病ラットにおけるxanthine oxidase阻害は圧過負荷誘発拡張機能障害を減弱させる(Inhibition of Xanthine Oxidase in Type 2 Diabetic Rats Ameliorates Pressure Overload-induced Diastolic Dysfunction)

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抄録集 ( (一社)日本循環器学会 )  83回   OJ40 - 9  2019.03

エピジェネティクスにおけるNon-coding RNA 糖尿病性心筋症の重要因子であるAMP deaminaseの新規microRNA介在性制御(Non-coding RNAs as Regulators in Epigenetics Novel microRNA-mediated Regulation of AMP Deaminase, a Key Player in Diabetic Cardiomyopathy)

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抄録集 ( (一社)日本循環器学会 )  83回   SY14 - 4  2019.03

Follow-up and prognosis of Kawasaki disease without coronary artery sequelae in adult

Kyuma Michifumi, Tatekoshi Yuki, Matsumoto Tamaki, Nishisato Kimio, Nishimura Mitsuhiro

Shinzo ( Japan Heart Foundation )  50 ( 12 ) 1289 - 1293  2018.12  [Refereed]

Article, review, commentary, editorial, etc. (scientific journal)  

　View Summary

背景および目的：成人期に達した川崎病既往者の冠動脈後遺症病変の長期的変化については，長い間議論が継続しているにもかかわらず，いまだに一定の見解に至っていない．冠動脈後遺症を伴う川崎病既往者はもちろんのこと，冠動脈後遺症を伴わない川崎病既往者においても成人期の急性冠症候群発症の報告が散見されるため，当院での成人期川崎病，特に冠動脈後遺症を伴わない症例に着目し，その追跡状況およびその予後を調査した． 方法：2017年12月時点で20歳以上の当科受診歴のある川崎病既往患者を抽出した．当院小児科より成人科移行として紹介された56例，または産科より川崎病既往のため心機能および冠動脈瘤評価目的で紹介された9例の計65例を検討した． 結果：当科最終通院時点での年齢は平均25.9歳，予後調査時点での平均年齢は33.9歳であった．川崎病診断後，急性期に静注用免疫グロブリン（IVIG）療法が確認できた症例は8例，アスピリン内服のみの症例が23例であった．IVIG施行を確認しえた8症例は1986年以降に発症の症例で，冠動脈瘤形成を1例に認めるが，急性期一過性冠動脈拡大，退縮は認めなかった．冠動脈後遺症を伴わない川崎病既往者57例中，予後調査時点で連絡可能であった全51例に心臓突然死，急性冠症候群の発症は認めなかった． 結論：現在までに当科受診の冠動脈後遺症を伴わない川崎病既往患者に心臓突然死および急性冠症候群の発症を認めてはいないが，近年これらの報告が散見されるため，そのリスクベネフィットを十分説明したうえでの追跡が重要であると思われた．

DOI CiNii

miR301b-mediated upregulation of AMP deaminase contributes to ATP depletion and DM cardiomyopathy

Yuki Tatekoshi, Masaya Tanno, Takayuki Miki, Atsushi Kuno, Toshiyuki Yano, Tatsuya Sato, Wataru Ohwada, Koki Abe, Hiroto Oshima, Masashi Mizuno, Tetsuji Miura

The 1st JCS Council Forum on Basic CardioVascular Research Program   P5-5  2018.01

Authorship：   Lead author

Research paper, summary (national, other academic conference)  

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  2017.11

Authorship：   Lead author

Research paper, summary (international conference)  

　View Summary

0

Upregulation of AMP deaminase in the vicinity of the SR via translational regulation by miR-301b contributes to diabetic cardiomyopathy

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

The 21st Annual Scientific Meeting of the Japanese Heart Failure Society Program   #O22-3  2017.10

Authorship：   Lead author

Research paper, summary (national, other academic conference)  

循環器内科学 心不全の発症進展におけるAMPデアミナーゼの役割

舘越 勇輝, 丹野 雅也

医学のあゆみ ( 医歯薬出版(株) )  262 ( 3 ) 243 - 244  2017.07

Authorship：   Lead author

Toll様受容体の活性化により2型糖尿病における心筋梗塞後のAKIに対する腎臓の感受性が増大する(Increased Renal Susceptibility to AKI after Myocardial Infarction in Type 2 Diabetes is Mediated by Augmented Activation of Toll-like Receptors)

大野 紘平, 久野 篤史, 三木 隆幸, 丹野 雅也, 矢野 俊之, 大和田 渉, 木村 幸滋, 安部 功記, 中田 圭, 舘越 勇輝, 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 )  81回   PJ - 594  2017.03

糖尿病性腎症による末期腎不全に至ってから診断されたCushing病の1例

高橋 遼, 舘越 勇輝, 茂庭 仁人, 西田 絢一, 矢野 俊之, 古橋 眞人, 三木 隆幸, 三浦 哲嗣

日本内分泌学会雑誌 ( (一社)日本内分泌学会 )  92 ( S.Branc ) 13 - 13  2016.12

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  2016.11

Research paper, summary (international conference)  

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  2016.09

Research paper, summary (international conference)  

DOI

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  2016.08

Research paper, summary (international conference)  

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  2016.07

Research paper, summary (international conference)  

糖尿病が腎虚血再灌流障害に及ぼす影響 オートファジーとの関連

村椿 真悟, 久野 篤史, 大野 紘平, 丹野 雅也, 矢野 俊之, 水野 雅司, 西沢 慶太郎, 大和田 渉, 舘越 勇輝, 中田 圭, 三木 隆幸, 三浦 哲嗣

日本腎臓学会誌 ( (一社)日本腎臓学会 )  58 ( 3 ) 276 - 276  2016.05

Increased activity of AMPdeaminase by decreased interaction with PGM1 and depletion of F1,6P: a novel mechanism of diabetic cardiomyopathy

Yuki Tatekoshi, Hidemichi Kouzu, Masaya Tanno, Atsushi Kuno, Satoko, Ishikawa Toshiyuki Yano, Takayuki Miki, Makoto Ogasawara, Toshiyuki Tobisawa, Kouhei Ono, Shingo Muratsubaki Keitaro, Nishizawa Tetsuji Miura

2016 XXII ISHR World Congress Program   WE-009  2016.04

Authorship：   Lead author

Research paper, summary (international conference)  

糖尿病心臓のAMP deaminaseの活性化においては翻訳後修飾ではなくfructose 1,6-diphosphateの枯渇が主要な役割を果たす(Depletion of Fructose 1,6-diphosphate but not Post-translational Modification Plays a Major Role in Activation of AMP Deaminase in Diabetic Hearts)

Tatekoshi Yuki, Kouzu Hidemichi, Tanno Masaya, Kuno Atsushi, Ishikawa Satoko, Yano Toshiyuki, Miki Takayuki, Ogasawara Makoto, Tobisawa Toshiyuki, Ono Kouhei, Muratsubaki Shingo, Nishizawa Keitaro, Miura Tetsuji

Circulation Journal ( (一社)日本循環器学会 )  80 ( Suppl.I ) 1115 - 1115  2016.03

J-GLOBAL

DPP-4阻害薬かSGLT-2阻害薬かの選択—DPP-4 inhibitors and SGLT-2 inhibitors in diabetes : how to choose?—薬剤選択の分岐点

三木 隆幸, 中田 圭, 舘越 勇輝

循環器内科 = Cardioangiology / 循環器内科編集委員会 編 ( 科学評論社 )  78 ( 6 ) 616 - 622  2015.12

CiNii

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

J-GLOBAL

IgA型多発性骨髄腫に伴うacute light chain tubulopathyの一例

瀬野 結, 田中 希尚, 舘越 勇輝, 青山 ちひろ, 大野 紘平, 古橋 眞人, 吉田 英昭, 坂本 孝志, 小川 弥生

日本腎臓学会誌 ( (一社)日本腎臓学会 )  56 ( 6 ) 877 - 877  2014.08

Complex cardiac injuries by blunt chest trauma by car crash including coronary dissection, huge thrombus, tricuspid valve and pericardial rupture

Yuki Tatekoshi, Nobuaki Kokubu, Mamoru Hase, Atusko Muranaka, Junichi Nishida Satoshi Yuda, Kazutoshi Tachibana, Yasuko Miyaki, Akiyoshi Hashimoto Nobuhiro, Takagi Kazufumi Tsuchihashi, Tetsuya Higami, Tetsuji Miura

EuroPCR 2014 Scientific Program   ACS without atherostenosis ( Clinical Cases )  2014.05

Authorship：   Lead author

Research paper, summary (international conference)  

交通外傷性右冠動脈解離・心膜損傷・三尖弁閉鎖不全症の1例

舘越 勇輝, 小笠原 惇, 村中 敦子, 湯田 聡, 土橋 和文, 橘 一俊, 宮木 靖子, 高木 伸之, 樋上 哲哉, 三浦 哲嗣

超音波医学 ( (公社)日本超音波医学会 )  41 ( Suppl. ) S499 - S499  2014.04

Authorship：   Lead author

Research paper, summary (national, other academic conference)  

交通外傷性右冠動脈解離・心膜損傷・三尖弁閉鎖不全症の1例

舘越 勇輝, 小笠原 惇, 村中 敦子, 湯田 聡, 長谷 守, 橋本 暁佳, 土橋 和文, 橘 一俊, 宮木 靖子, 高木 伸之, 樋上 哲哉, 三浦 哲嗣

超音波医学 ( (公社)日本超音波医学会 )  41 ( 1 ) 50 - 50  2014.01

Authorship：   Lead author

Research paper, summary (national, other academic conference)