当前位置： SCI文献检索 > JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY期刊下所有文献 > Soluble epoxide hydrolase activation by S-nitrosation contributes to cardiac ischemia-reperfusion injury.

Soluble epoxide hydrolase activation by S-nitrosation contributes to cardiac ischemia-reperfusion injury.

Abstract：

:Cardiac ischemia-reperfusion (I/R) injury always accompanies recanalization treatment for myocardial infarction. Here we found soluble epoxide hydrolase (sEH), which metabolizes cardioprotective epoxyeicosatrienoic acids into less effective diols, was rapidly activated during myocardial reperfusion in both mouse and rat models in expression-independent manner. Similar activation was mimicked by nitric oxide (NO) donor dose-dependently in vitro, along with an obvious induction of sEH S-nitrosation, a short-term post-translational modification, which diminished in sEH Cys-141-Ala mutant. In vivo, I/R induced sEH S-nitrosation could be reversed by NO synthase inhibitor L-NAME, with protective effect on cardiac dysfunction, which however vanished in sEH-/- mice. Further, a protective effect against I/R injury in the initial phase of reperfusion was observed in eNOS-/- mice, indicating inhibition of NO as a sEH-based cardioprotective in early time of I/R injury. Besides, sEH inhibitor directly targeting on activated sEH during cardiac reperfusion significant reduced infarct size after I/R in vivo. In summary, our findings show the critical role of sEH S-nitrosation in cardiac I/R injury and inhibiting sEH S-nitrosation may be a new therapeutic strategy clinically.

journal_name

J Mol Cell Cardiol

journal_title

Journal of molecular and cellular cardiology

authors

Ding Y,Li Y,Zhang X,He J,Lu D,Fang X,Wang Y,Wang J,Zhang Y,Qiao X,Gan LM,Chen C,Zhu Y

doi

10.1016/j.yjmcc.2017.07.006

subject

Has Abstract

pub_date

2017-09-01 00:00:00

pages

70-79

eissn

0022-2828

issn

1095-8584

pii

S0022-2828(17)30160-8

journal_volume

110

pub_type

杂志文章

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