Misc - 丹野　雅也

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

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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

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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

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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.

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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.

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