論文 - 丹野　雅也

Ito電流は肥満2型糖尿病においてKv4.2およびKChIP2のダウンレギュレーションにより心内膜下で選択的に低下する(The Ito Current is Reduced Selectively in the Subendocardium by Downregulation of Kv4.2 and KChIP2 in Obese Type 2 Diabetes)

Sato Tatsuya, Miki Takayuki, Tanno Masaya, Kuno Atsushi, Kobayashi Takeshi, Kouzu Hidemichi, Itoh Takahito, Sunaga Daisuke, Murase Hiromichi, Ishikawa Satoko, Miura Tetsuji, Tohse Noritsugu

Circulation Journal ( (一社)日本循環器学会 )  76 ( Suppl.I ) 1592 - 1592  2012年03月

Ser9位のGSK-3βのリン酸化はミトコンドリアへの移行を阻害し、ミトコンドリアによる致死性ROS産生を減弱する(Phosphorylation of GSK-3β at Ser9 Inhibits Its Translocation to Mitochondria and Attenuates Lethal ROS Production by Mitochondria)

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

Circulation Journal ( (一社)日本循環器学会 )  76 ( Suppl.I ) 943 - 943  2012年03月

Role of ER stress in ventricular contractile dysfunction in type 2 diabetes.

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

PloS one   7 ( 6 ) e39893  2012年  [査読有り]

DOI PubMed

Resveratrol ameliorates muscular pathology in the dystrophic mdx mouse, a model for Duchenne muscular dystrophy.

Hori YS, Kuno A, Hosoda R, Tanno M, Miura T, Shimamoto K, Horio Y

The Journal of pharmacology and experimental therapeutics   338 ( 3 ) 784 - 794  2011年09月  [査読有り]

DOI PubMed

軽度の心室機能不全とadrenalin刺激に対する反応鈍化は肥満2型糖尿病における心筋梗塞後の高い死亡率の素因となる(Slight Ventricular Dysfunction and Blunted Response to Adrenergic Stimulation Predispose to Higher Mortality after Infarction in Obese Type 2 Diabetes)

Takada Akifumi, Miki Takayuki, Tanno Masaya, Kuno Atsushi, Kohzu Hidemichi, Itoh Takahito, Satoh Tatsuya, Sunaga Daisuke, Miura Tetsuji

Circulation Journal ( (一社)日本循環器学会 )  75 ( Suppl.I ) 44 - 44  2011年03月

2型糖尿病におけるerythropoietinに対する心筋反応欠如の根底にはミトコンドリア膜透過性遷移孔のERストレス介在性の異常調節がある(ER Stress-mediated Dysregulation of the Mitochondrial Permeability Transition Pore Underlies Loss of Myocardial Response to Erythropoietin in Type 2 Diabetes)

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

Circulation Journal ( (一社)日本循環器学会 )  75 ( Suppl.I ) 17 - 17  2011年03月

Hypertensive hypertrophied myocardium is vulnerable to infarction and refractory to erythropoietin-induced protection.

Yano T, Miki T, Tanno M, Kuno A, Itoh T, Takada A, Sato T, Kouzu H, Shimamoto K, Miura T

Hypertension (Dallas, Tex. : 1979)   57 ( 1 ) 110 - 115  2011年01月  [査読有り]

DOI PubMed

Erythropoietin (EPO) affords more potent cardioprotection by activation of distinct signaling to mitochondrial kinases compared with carbamylated EPO.

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

Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy ( 5-6 )  24   401 - 408  2010年12月  [査読有り]

DOI PubMed

Roles of phospho-GSK-3β in myocardial protection afforded by activation of the mitochondrial K ATP channel.

Terashima Y, Sato T, Yano T, Maas O, Itoh T, Miki T, Tanno M, Kuno A, Shimamoto K, Miura T

Journal of molecular and cellular cardiology   49 ( 5 ) 762 - 770  2010年11月  [査読有り]

DOI PubMed

Mitochondrial kinase signalling pathways in myocardial protection from ischaemia/reperfusion-induced necrosis

Tetsuji Miura, Masaya Tanno, Tatsuya Sato

CARDIOVASCULAR RESEARCH ( OXFORD UNIV PRESS )  88 ( 1 ) 7 - 15  2010年10月  [査読有り]

　概要を見る

Multiple cardioprotective signal pathways that are activated by ischaemic preconditioning (IPC) and those by IPC mimetics converge on mitochondria. Recent studies have shown that pools of Akt, protein kinase C-epsilon, extracellular-regulated kinases, glycogen synthase kinase-3 beta (GSK-3 beta), and hexokinases (HK) I and II, are localized in mitochondria in addition to their pools in the cytosol. Accumulating evidence indicates that such 'mitochondrial protein kinases' receive signals from cytosolic molecules and enhance tolerance of myocytes to injury. Proteomic analyses suggest that these kinases form complexes with each other and with subunit proteins of the mitochondrial permeability transition pore (mPTP). Functional relationships between the protein kinases in mitochondria have not been fully clarified, but GSK-3 beta and HKs appear to be at the end of the signal pathways and directly responsible for inhibition of opening of the mPTP and, thus, for myocyte protection from necrosis. In this review, recent findings supporting roles of mitochondrial protein kinases in protection from myocardial necrosis after ischaemia/reperfusion are summarized and discussed.

DOI PubMed

Protein deacetylase SIRT1 in the cytoplasm promotes nerve growth factor-induced neurite outgrowth in PC12 cells.

Sugino T, Maruyama M, Tanno M, Kuno A, Houkin K, Horio Y

FEBS letters   584 ( 13 ) 2821 - 2826  2010年07月  [査読有り]

DOI PubMed

Protein deacetylase SIRT1 in the cytoplasm promotes nerve growth factor-induced neurite outgrowth in PC12 cells

Toshiya Sugino, Mitsuhisa Maruyama, Masaya Tanno, Atsushi Kuno, Kiyohiro Houkin, Yoshiyuki Horio

FEBS LETTERS ( WILEY )  584 ( 13 ) 2821 - 2826  2010年07月  [査読有り]

　概要を見る

SIRT1, a NAD(+)-dependent protein deacetylase, is known to have neural functions. However, despite its cytoplasmic expression in some neural cells, its cytoplasmic function, if any, is unknown. Here we found that PC12 (pheochromocytoma) cells expressed SIRT1 in the cytoplasm. Nerve growth factor (NGF)-induced neurite outgrowth of these cells was promoted by activators of SIRT1, while inhibitors of SIRT1 or SIRT1-siRNA significantly inhibited it. The overexpression of a mutant SIRT1 that localised to the cytoplasm but not the nucleus enhanced the NGF-dependent neurite outgrowth, and a cytoplasmic dominant-negative SIRT1 suppressed it. Thus, cytoplasmic SIRT1 increases the NGF-induced neurite outgrowth of PC12 cells. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

DOI

Mitochondria and GSK-3beta in cardioprotection against ischemia/reperfusion injury.

Miura T, Tanno M

Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy ( 3 )  24   255 - 263  2010年06月  [査読有り]

DOI PubMed

Induction of manganese superoxide dismutase by nuclear translocation and activation of SIRT1 promotes cell survival in chronic heart failure.

Tanno M, Kuno A, Yano T, Miura T, Hisahara S, Ishikawa S, Shimamoto K, Horio Y

The Journal of biological chemistry   285 ( 11 ) 8375 - 8382  2010年03月  [査読有り]

DOI PubMed

Angiotensin II type 1 receptor-mediated upregulation of calcineurin activity underlies impairment of cardioprotective signaling in diabetic hearts.

Hotta H, Miura T, Miki T, Togashi N, Maeda T, Kim SJ, Tanno M, Yano T, Kuno A, Itoh T, Satoh T, Terashima Y, Ishikawa S, Shimamoto K

Circulation research   106 ( 1 ) 129 - 132  2010年01月  [査読有り]

DOI PubMed

Endoplasmic reticulum stress in diabetic hearts abolishes erythropoietin-induced myocardial protection by impairment of phospho-glycogen synthase kinase-3beta-mediated suppression of mitochondrial permeability transition.

Miki T, Miura T, Hotta H, Tanno M, Yano T, Sato T, Terashima Y, Takada A, Ishikawa S, Shimamoto K

Diabetes ( 12 )  58   2863 - 2872  2009年12月  [査読有り]

DOI PubMed

Roles of Cx43-associated protein kinases in suppression of gap junction-mediated chemical coupling by ischemic preconditioning.

Naitoh K, Yano T, Miura T, Itoh T, Miki T, Tanno M, Sato T, Hotta H, Terashima Y, Shimamoto K

American journal of physiology. Heart and circulatory physiology ( 2 )  296   H396 - 403  2009年02月  [査読有り]

DOI PubMed

Ser9 phosphorylation of mitochondrial GSK-3beta is a primary mechanism of cardiomyocyte protection by erythropoietin against oxidant-induced apoptosis.

Ohori K, Miura T, Tanno M, Miki T, Sato T, Ishikawa S, Horio Y, Shimamoto K

American journal of physiology. Heart and circulatory physiology ( 5 )  295   H2079 - 86  2008年11月  [査読有り]

DOI PubMed

Histone deacetylase SIRT1 modulates neuronal differentiation by its nuclear translocation

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

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA ( NATL ACAD SCIENCES )  105 ( 40 ) 15599 - 15604  2008年10月  [査読有り]

　概要を見る

Neural precursor cells (NPCs) differentiate into neurons, astrocytes, and oligodendrocytes in response to intrinsic and extrinsic changes. Notch signals maintain undifferentiated NPCs, but the mechanisms underlying the neuronal differentiation are largely unknown. We show that SIRT1, an NAD(+)-dependent histone deacetylase, modulates neuronal differentiation. SIRT1 was found in the cytoplasm of embryonic and adult NPCs and was transiently localized in the nucleus in response to differentiation stimulus. SIRT1 started to translocate into the nucleus within 10 min after the transfer of NPCs into differentiation conditions, stayed in the nucleus, and then gradually retranslocated to the cytoplasm after several hours. The number of neurospheres that generated Tuj1(+) neurons was significantly decreased by pharmacological inhibitors of SIRT1, dominant-negative SIRT1 and SIRT1-siRNA, whereas overexpression of SIRT1, but not that of cytoplasm-localized mutant SIRT1, enhanced neuronal differentiation and decreased Hes1 expression. Expression of SIRT1-siRNA impaired neuronal differentiation and migration of NPCs into the cortical plate in the embryonic brain. Nuclear receptor corepressor (N-CoR), which has been reported to bind SIRT1, promoted neuronal differentiation and synergistically increased the number of Tuj1(+) neurons with SIRT1, and both bound the Hes1 promoter region in differentiating NPCs. Hes1 transactivation by Notch1 was inhibited by SIRT1 and/or N-CoR. Our study indicated that SIRT1 is a player of repressing Notch1-Hes1 signaling pathway, and its transient translocation into the nucleus may have a role in the differentiation of NPCs.

DOI

Adenine nucleotide translocator, a mitochondrial carrier protein, and fate of cardiomyocytes after ischaemia/reperfusion

Masaya Tanno, Tetsuji Miura

CARDIOVASCULAR RESEARCH ( OXFORD UNIV PRESS )  80 ( 1 ) 1 - 2  2008年10月  [査読有り]

DOI PubMed