C1q/tumor necrosis factor-related protein-3, a newly identified adipokine, is a novel antiapoptotic, proangiogenic, and cardioprotective molecule in the ischemic mouse heart

Obesity and diabetes mellitus adversely affect postischemic heart remodeling via incompletely understood mechanisms. C1q/tumor necrosis factor-related protein-3 (CTRP3) is a newly identified adipokine exerting beneficial metabolic regulation, similar to adiponectin. The aim of the present study was...

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Published in:Circulation (New York, N.Y.) N.Y.), 2012-06, Vol.125 (25), p.3159-3169
Main Authors: Yi, Wei, Sun, Yang, Yuan, Yuexing, Lau, Wayne Bond, Zheng, Qijun, Wang, Xiaoliang, Wang, Yajing, Shang, Xiying, Gao, Erhe, Koch, Walter J, Ma, Xin-Liang
Format: Article
Language:English
Subjects:
Adipokines - antagonists & inhibitors
Adipokines - physiology
Adipokines - therapeutic use
Angiogenesis Inducing Agents - metabolism
Angiogenesis Inducing Agents - therapeutic use
Animals
Apoptosis Regulatory Proteins - antagonists & inhibitors
Apoptosis Regulatory Proteins - physiology
Apoptosis Regulatory Proteins - therapeutic use
Cardiotonic Agents - metabolism
Cardiotonic Agents - therapeutic use
Gene Knockdown Techniques - methods
Human Umbilical Vein Endothelial Cells
Humans
Male
Mice
Mice, Inbred C57BL
Myocardial Ischemia - genetics
Myocardial Ischemia - metabolism
Myocardial Ischemia - prevention & control
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Summary:Obesity and diabetes mellitus adversely affect postischemic heart remodeling via incompletely understood mechanisms. C1q/tumor necrosis factor-related protein-3 (CTRP3) is a newly identified adipokine exerting beneficial metabolic regulation, similar to adiponectin. The aim of the present study was to determine whether CTRP3 may regulate postischemic cardiac remodeling and cardiac dysfunction, and, if so, to elucidate the underlying mechanisms. Male adult mice were subjected to myocardial infarction (MI) via left anterior descending coronary artery occlusion. Both the effect of MI on endogenous CTRP3 expression/production and the effect of exogenous CTRP3 (adenovirus or recombinant CTRP3) replenishment on MI injury were investigated. MI significantly inhibited adipocyte CTRP3 expression and reduced the plasma CTRP3 level, reaching a nadir 3 days after MI. CTRP3 replenishment improved survival rate (P
ISSN:0009-7322
1524-4539
DOI:10.1161/circulationaha.112.099937