Cardioprotective effects of adipokine apelin on myocardial infarction
Angiogenesis plays an important role in myocardial infarction.Apelin and its natural receptor (angiotensin Ⅱ receptor-like 1, AGTRL-1 or APLNR) induce sprouting of endothelial cells in an autocrine or paracrine manner.The aim of this study is to investigate whether apelin can improve the cardiac function after myocardial infarction by increasing angiogenesis in infarcted myocardium.Left ventricular end-diastolic pressure (LVEDP), left ventricular end systolic pressure (LVESP), left ventricular developed pressure (LVDP), maximal left ventricular pressure development (±LVdp/dtmax), infarct size, and angiogenesis were evaluated to analyze the cardioprotective effects of apelin on ischemic myocardium.Assays of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, 5-bromo-2”-deoxyuridine incorporation, wound healing, transwells, and tube formation were used to detect the effects of apelin on proliferation, migration, and chemotaxis of cardiac microvascular endothelial cells.Fluorescein isothiocyanate-labeled bovine serum albumin penetrating through monolayered cardiac microvascular endothelial cells was measured to evaluate the effects of apelin on permeability of microvascular endothelial cells.In vivo results showed that apelin increased ±LV dp/dtmax and LVESP values, decreased LVEDP values (all p <0.05), and promoted angiogenesis in rat heart after ligation of the left anterior descending coronary artery.In vitro results showed that apelin dose-dependently enhanced proliferation, migration, chemotaxis, and tube formation, but not permeability of cardiac microvascular endothelial cells.Apelin also increased the expression of vascular endothelial growth factor receptors-2 (VEGFR2) and the endothelium-specific receptor tyrosine kinase (Tie-2) in cardiac microvascular endothelial cells.These results indicated that apelin played a protective role in myocardial infarction through promoting angiogenesis and decreasing permeability of microvascular endothelial cells via upregulating the expression of VEGFR2 and Tie-2 in cardiac microvascular endothelial cells.
Apelin Myocardial infarction Endothelial cell Angiogenesis
Bao-Hai Zhang Cai-Xia Guo Hong-Xia Wang Ling-Qiao Lu Ya-Jie Wang Li-Ke Zhang Feng-He Du Xiang-Jun Zeng
The Department of Pathophysiology, Capital Medical University, Beijing 100069, China;Division of Car Division of Cardiology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China The Department of Pathophysiology, Capital Medical University, Beijing 100069, China Laboratory of Clinical Medical Research, Beijing Tiantan Hospital, Capital Medical University, Beiji
国内会议
北京
英文
142-152
2015-08-01（万方平台首次上网日期，不代表论文的发表时间）