Papers - TANNO Masaya

Limitation of infarct size by erythropoietin is associated with translocation of Akt to the mitochondria after reperfusion.

Kobayashi H, Miura T, Ishida H, Miki T, Tanno M, Yano T, Sato T, Hotta H, Shimamoto K

Clinical and experimental pharmacology & physiology ( 7 )  35   812 - 819  2008.07  [Refereed]

DOI PubMed

Modulation of the mitochondrial permeability transition pore complex in GSK-3beta-mediated myocardial protection.

Nishihara M, Miura T, Miki T, Tanno M, Yano T, Naitoh K, Ohori K, Hotta H, Terashima Y, Shimamoto K

Journal of molecular and cellular cardiology ( 5 )  43   564 - 570  2007.11  [Refereed]

DOI PubMed

Delta-opioid receptor activation before ischemia reduces gap junction permeability in ischemic myocardium by PKC-epsilon-mediated phosphorylation of connexin 43.

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

American journal of physiology. Heart and circulatory physiology ( 3 )  293   H1425 - 31  2007.09  [Refereed]

DOI PubMed

Protecting ischemic hearts by modulation of SR calcium handling

Masaya Tanno, Tetsuji Miura

CARDIOVASCULAR RESEARCH ( ELSEVIER SCIENCE BV )  75 ( 3 ) 453 - 454  2007.08  [Refereed]

DOI PubMed

Nucleocytoplasmic shuttling of the NAD+-dependent histone deacetylase SIRT1.

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

The Journal of biological chemistry ( 9 )  282   6823 - 6832  2007.03  [Refereed]

DOI PubMed

Impairment of cardioprotective PI3K-Akt signaling by post-infarct ventricular remodeling is compensated by an ERK-mediated pathway.

Miki T, Miura T, Tanno M, Nishihara M, Naitoh K, Sato T, Takahashi A, Shimamoto K

Basic research in cardiology ( 2 )  102   163 - 170  2007.03  [Refereed]

DOI PubMed

Activation of ERK and suppression of calcineurin are interacting mechanisms of cardioprotection afforded by delta-opioid receptor activation.

Ikeda Y, Miura T, Sakamoto J, Miki T, Tanno M, Kobayashi H, Ohori K, Takahashi A, Shimamoto K

Basic research in cardiology ( 5 )  101   418 - 426  2006.09  [Refereed]

DOI PubMed

Erythropoietin affords additional cardioprotection to preconditioned hearts by enhanced phosphorylation of glycogen synthase kinase-3 beta.

Nishihara M, Miura T, Miki T, Sakamoto J, Tanno M, Kobayashi H, Ikeda Y, Ohori K, Takahashi A, Shimamoto K

American journal of physiology. Heart and circulatory physiology ( 2 )  291   H748 - 55  2006.08  [Refereed]

DOI PubMed

Alteration in erythropoietin-induced cardioprotective signaling by postinfarct ventricular remodeling.

Miki T, Miura T, Yano T, Takahashi A, Sakamoto J, Tanno M, Kobayashi H, Ikeda Y, Nishihara M, Naitoh K, Ohori K, Shimamoto K

The Journal of pharmacology and experimental therapeutics ( 1 )  317   68 - 75  2006.04  [Refereed]

DOI PubMed

Time window for the contribution of the delta-opioid receptor to cardioprotection by ischemic preconditioning in the rat heart

A Tsuchida, T Miura, M Tanno, Y Nozawa, H Kita, K Shimamoto

CARDIOVASCULAR DRUGS AND THERAPY ( SPRINGER )  12 ( 4 ) 365 - 373  1998.09  [Refereed]

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The present study aimed to examine (1) whether the role of the opioid receptor in ischemic preconditioning (PC) is consistent regardless of the duration of ischemic insult and (2) which opioid receptor subtype contributes to PC. In the first series of experiments, the effects of PC, a nonselective opioid receptor antagonist (naloxone), and their combination on the infarct size after various durations of ischemia were assessed. In anesthetized, open-chest rats, the coronary artery was occluded for 20, 30, or 40 minutes to induce infarction and was reperfused for 3 hours, PC was performed with two cycles of 5-minute ischemia followed by 5-minute reperfusion before the sustained ischemia. At 25 minutes before the ischemia, naloxone was injected alone or in combination with subsequent PC. Infarct size was determined by tetrazolium staining and was expressed as a percentage of the risk area size (%IS/RA). In the second series of experiments, the effects of a delta-receptor selective antagonist, naltrindole (NTI), and a kappa-receptor selective antagonist, nor-binaltrophimine (nor-BNI), on PC before 30-minute coronary occlusion were assessed. In untreated controls, %IS/RA was 53.1 +/- 3.2 after 20 minutes, 67.9 +/- 3.9 after 30 minutes, and 87.8 +/- 2.0 after 40 minutes of ischemia, respectively. PC significantly reduced %IS/RA after 20, 30, and 40 minutes of ischemia to 3.1 +/- 0.8, 12.8 +/- 1.1, and 42.1 +/- 4.3, respectively (P < 0.05 vs, each control). Naloxone (6 mg/kg) partially attenuated the protection afforded by PC when the sustained ischemia was 30 minutes (%IS/RA = 27.4 +/- 4.5; P < 0.05 vs. PC), but this inhibitory effect of naloxone was not detected when the duration of the ischemia was 20 or 40 minutes. NTI (10 mg/kg) also attenuated infarct size limitation by PC after 30 minutes of ischemia (%IS/RA = 25.6 +/- 3.7), but nor-BNI (10 mg/kg) failed to modify infarct size limitation by PC (%IS/RA = 13.3 +/- 3.2). The present results suggest that activation of the opioid delta-receptor partly contributes to preconditioning against infarction in the rat and that there may be a time window (at around 30 minutes after the onset of ischemia) for this opioid receptor-mediated protective mechanism.