Adiponectin regulates SR Ca2+ cycling following ischemia/reperfusion via sphingosine 1-phosphate-CaMKII signaling in mice

被引：30

作者：

Yan, Wenjun ^{[1
]}

Zhang, Fuyang ^{[1
]}

Zhang, Ronghuai ^{[1
]}

Zhang, Xing ^{[3
]}

Wang, Yanru ^{[4
]}

Zhou, Fen ^{[1
]}

Xia, Yunlong ^{[1
]}

Liu, Peilin ^{[1
]}

Gao, Chao ^{[1
]}

Wang, Han ^{[1
]}

Zhang, Lijian ^{[1
]}

Zhou, Jingjun ^{[3
]}

Gao, Feng ^{[3
]}

Gao, Erhe ^{[5
]}

Koch, Walter J. ^{[5
]}

Wang, Haichang ^{[1
]}

Cheng, Heping ^{[4
]}

Qu, Yan ^{[2
]}

Tao, Ling ^{[1
]}

机构：

[1] Fourth Mil Med Univ, Xijing Hosp, Dept Cardiol, Xian 710032, Peoples R China

[2] Fourth Mil Med Univ, Xijing Hosp, Dept Neurosurg, Xian 710032, Peoples R China

[3] Fourth Mil Med Univ, Sch Basic Med Sci, Dept Physiol, Xian 710032, Peoples R China

[4] Peking Univ, Inst Mol Med, Beijing 100083, Peoples R China

[5] Temple Univ, Ctr Translat Med, Sch Med, Philadelphia, PA 19107 USA

来源：

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY | 2014年 / 74卷

关键词：

Adiponectin; Myocardial ischetnia/reperfusion; Sphingosine; 1-phosphate; SERCA2; SARCOPLASMIC-RETICULUM; PROTEIN-KINASE; PLASMA-CONCENTRATIONS; INTERMITTENT HYPOXIA; CARDIAC-FUNCTION; CARDIOPROTECTION; REPERFUSION; INJURY; ISCHEMIA; RECEPTOR;

D O I：

10.1016/j.yjmcc.2014.05.010

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The adipocyte-secreted hormone adiponectin (APN) exerts protective effects on the heart under stress conditions. Recent studies have demonstrated that APN induces a marked Ca2+ influx in skeletal muscle. However, whether APN modulates [Ca2+](i) activity, especially [Ca2+](i) transients in cardiomyocytes, is still unknown. This study was designed to determine whether APN modulates [Ca2+](i) transients in cardiomyocytes. Adult male wild-type (WT) and APN knockout (APN KO) mice were subjected to myocardial ischemia/reperfusion (I/R, 30 min/30 min) injury. CaMKII-PLB phosphorylation and SR Ca2+-ATPase (SERCA2) activity were downregulated in I/R hearts of WF mice and further decreased in those of APN KO mice. Both the globular domain of APN and full-length APN significantly reversed the decrease in CaMKII-PLB phosphorylation and SERCA2 activity in WT and APN KO mice. Interestingly, compared with WT littermates, single myocytes isolated from APN KO mice had remarkably decreased [Ca2+](i) transients, cell shortening, and a prolonged Ca2+ decay rate. Further examination revealed that APN enhances SERCA2 activity via CaMKII-PLB signaling. In in vivo and in vitro experiments, both APN receptor 1/2 and SIP were necessary for the APN-stimulated CaMKII-PLB-SERCA2 activation. In addition, SIP activated CaMKII-PLB signaling in neonatal cardiomyocytes in a dose dependent manner and improved [Ca2+](i) transients in APN KO myocytes via the SIP receptor (S1PR1/3). Further in vivo experiments revealed that pharmacological inhibition of S1PR1/3 and SERCA2 siRNA suppressed APN-mediated cardioprotection during I/R. These data demonstrate that SIP is a novel regulator of SERCA2 that activates CaMKII-PLB signaling and mediates APN-induced cardioprotection. (C) 2014 Elsevier Ltd. All rights reserved.

引用

页码：183 / 192

页数：10

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