Soluble epoxide hydrolase activation by S-nitrosation contributes to cardiac ischemia-reperfusion injury | |
Ding, Yuzhu3; Li, Yazi2; Zhang, Xu5; He, Jinlong5; Lu, Dong4; Fang, Xuan3; Wang, Yuchen3; Wang, Jiaxing3; Zhang, Yuying2; Qiao, Xinhua2 | |
刊名 | JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY |
2017-09 | |
卷号 | 110页码:70-79 |
关键词 | Epoxyeicosatrienoic acid Ischemia-reperfusion Nitric oxide S-nitrosation Soluble epoxide hydrolase |
ISSN号 | 0022-2828 |
DOI | 10.1016/j.yjmcc.2017.07.006 |
文献子类 | Article |
英文摘要 | 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. (C) 2017 Elsevier Ltd. All rights reserved. |
资助项目 | Ministry of Science and Technology of China[2016YFC0903000] ; Ministry of Science and Technology of China[2015BAI08B01] ; National Natural Science Foundation of China[81420108003] ; National Natural Science Foundation of China[31225012] ; National Natural Science Foundation of China[81400320] ; National Natural Science Foundation of China[91539108] ; Peking University-AstraZeneca Collaborative grant[SEML-89HH3C] |
WOS关键词 | ENDOTHELIUM IN-VITRO ; EPOXYEICOSATRIENOIC ACIDS ; ARACHIDONIC-ACID ; INFARCT SIZE ; NITROSYLATION ; RATS ; INHIBITION ; MECHANISM ; HEART ; VIVO |
WOS研究方向 | Cardiovascular System & Cardiology ; Cell Biology |
语种 | 英语 |
出版者 | ELSEVIER SCI LTD |
WOS记录号 | WOS:000411422500008 |
内容类型 | 期刊论文 |
源URL | [http://119.78.100.183/handle/2S10ELR8/272496] |
专题 | 药物发现与设计中心 |
通讯作者 | Chen, Chang; Zhu, Yi |
作者单位 | 1.AstraZeneca R&D, Innovat Med & Early Dev, SE-43183 Molndal, Sweden 2.Chinese Acad Sci, Natl Lab Biomacromol, Inst Biophys, Beijing 100101, Peoples R China; 3.Peking Univ, Dept Physiol & Pathophysiol, Hlth Sci Ctr, Beijing 100191, Peoples R China; 4.Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai 201203, Peoples R China; 5.Tianjin Med Univ, Tianjin Key Lab Metab Dis, Collaborat Innovat Ctr Tianjin Med Epigenet, Dept Physiol & Pathophysiol, Tianjin 300070, Peoples R China; |
推荐引用方式 GB/T 7714 | Ding, Yuzhu,Li, Yazi,Zhang, Xu,et al. Soluble epoxide hydrolase activation by S-nitrosation contributes to cardiac ischemia-reperfusion injury[J]. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY,2017,110:70-79. |
APA | Ding, Yuzhu.,Li, Yazi.,Zhang, Xu.,He, Jinlong.,Lu, Dong.,...&Zhu, Yi.(2017).Soluble epoxide hydrolase activation by S-nitrosation contributes to cardiac ischemia-reperfusion injury.JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY,110,70-79. |
MLA | Ding, Yuzhu,et al."Soluble epoxide hydrolase activation by S-nitrosation contributes to cardiac ischemia-reperfusion injury".JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY 110(2017):70-79. |
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