中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Cardioprotection of post-ischemic moderate ROS against ischemia/reperfusion via STAT3-induced the inhibition of MCU opening

文献类型:期刊论文

作者Wu, Lan1,3,4; Huang, Gang1,4; Tan, Ji-Liang2; Chen, Zhong-Yan2; ,
刊名BASIC RESEARCH IN CARDIOLOGY
出版日期2019
卷号114期号:5页码:39
关键词Post-ischemic moderate ROS Hydrogen peroxide postconditioning Mitochondrial Ca2+ concentration Cardiac contraction Signal transducer and activator of transcription 3 Mitochondrial calcium uniporter
ISSN号0300-8428
DOI10.1007/s00395-019-0747-9
文献子类Article
英文摘要Enhanced reactive oxygen species (ROS) at the beginning of reperfusion activated signal transducer and activator of transcription 3 (STAT3) in intermittent hypobaric hypoxia (IHH)-afforded cardioprotection against ischemia/reperfusion (I/R). However, its mechanism remains largely unknown. This study aimed to investigate the role and the downstream of STAT3 in exogenous enhanced post-ischemic ROS-induced cardioprotection using the model of moderate hydrogen peroxide postconditioning (H2O2PoC) mimicking endogenous ROS in IHH. Moderate H2O2PoC not only improved the post-ischemic myocardial contractile recovery and reduced the infarct size in isolated rat I/R hearts, but also alleviated mitochondrial calcium overload and ameliorated Ca2+ transients, cell contraction, and mitochondrial membrane potential in rat I/R cardiomyocytes. However, the cardioprotective effects of moderate H2O2PoC were abrogated by Janus kinase 2 (JAK2)/STAT3 inhibitor AG490 in rat hearts as well as adenovirus-delivered short hairpin RNA specific for STAT3 and the opener of mitochondrial calcium uniporter (MCU) spermine in rat cardiomyocytes. Notably, the moderate H2O2PoC-afforded cardioprotection abrogated by spermine could be rescued by STAT3 over-expression with adenovirus in rat I/R cardiomyocytes. Besides, moderate H2O2PoC enhanced mitochondrial STAT3 expression during I/R. A co-localization/interaction of STAT3 or phospho-STAT3(ser727) and MCU was observed in rat cardiomyocytes with moderate H2O2PoC at 5 and 30 min of reperfusion but not in rat I/R cardiomyocytes. Further, STAT3 interacted with the N-terminal domain (NTD) of MCU in rat cardiomyocytes with moderate H2O2PoC. These findings indicated that post-ischemic moderate ROS activate STAT3 against cardiac I/R by inhibiting MCU opening via its interaction with the NTD of MCU to alleviate mitochondrial calcium overload.
学科主题Cardiovascular System & Cardiology
WOS关键词MITOCHONDRIAL CALCIUM UNIPORTER ; NECROSIS-FACTOR-ALPHA ; REPERFUSION INJURY ; CA2+ OVERLOAD ; AFFORDED CARDIOPROTECTION ; PROTECTS CARDIOMYOCYTES ; SIGNAL-TRANSDUCTION ; HYDROGEN-PEROXIDE ; ISCHEMIA ; STRESS
语种英语
WOS记录号WOS:000483638200001
出版者SPRINGER HEIDELBERG
版本出版稿
源URL[http://202.127.25.144/handle/331004/533]  
专题中国科学院上海生命科学研究院营养科学研究所
作者单位1.Shanghai Univ Med & Hlth Sci, Sch Basic Med Sci, Shanghai 201318, Peoples R China;
2.Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai Inst Nutr & Hlth, Lab Mol Cardiol, Shanghai 200031, Peoples R China;
3.Shanghai Univ Med & Hlth Sci, Affiliated Zhoupu Hosp, Dept Cardiol, Shanghai 201318, Peoples R China,
4.Shanghai Univ Med & Hlth Sci, Shanghai Key Lab Mol Imaging, Shanghai 201318, Peoples R China;
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GB/T 7714
Wu, Lan,Huang, Gang,Tan, Ji-Liang,et al. Cardioprotection of post-ischemic moderate ROS against ischemia/reperfusion via STAT3-induced the inhibition of MCU opening[J]. BASIC RESEARCH IN CARDIOLOGY,2019,114(5):39.
APA Wu, Lan,Huang, Gang,Tan, Ji-Liang,Chen, Zhong-Yan,&,.(2019).Cardioprotection of post-ischemic moderate ROS against ischemia/reperfusion via STAT3-induced the inhibition of MCU opening.BASIC RESEARCH IN CARDIOLOGY,114(5),39.
MLA Wu, Lan,et al."Cardioprotection of post-ischemic moderate ROS against ischemia/reperfusion via STAT3-induced the inhibition of MCU opening".BASIC RESEARCH IN CARDIOLOGY 114.5(2019):39.

入库方式: OAI收割

来源:上海营养与健康研究所

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