Cardioprotective effects of adipokine apelin on myocardial infarction
Cardioprotective effects of adipokine apelin on myocardial infarction
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脂肪因子 apelin 对心肌梗死的心脏保护作用
DOI：
10.1007/s00380-013-0425-z
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发表时间：
2014-09
影响因子：
1.5
通讯作者：
Zeng, Xiang-Jun
中科院分区：
文献类型：
--
作者：
Wang, Ya-Jie;Zhang, Li-Ke;Du, Feng-He;Zeng, Xiang-Jun
血管生成在心肌梗塞中起着重要作用。 Apelin 及其天然受体（血管紧张素 II 受体样 1、AGTRL-1 或 APLNR）以自分泌或旁分泌方式诱导内皮细胞出芽。本研究的目的是探讨apelin是否可以通过增加梗塞心肌中的血管生成来改善心肌梗塞后的心功能。评估左心室舒张末压（LVEDP）、左心室收缩末压（LVESP）、左心室发展压（LVDP）、最大左心室发展压（±LVdp/dtmax）、梗塞面积和血管生成，分析apelin对缺血心肌的心脏保护作用。采用 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物、5-溴-2'-脱氧尿苷掺入、伤口愈合、Transwell 和管形成等检测来检测 apelin 对心脏微血管内皮细胞增殖、迁移和趋化性的影响。测定异硫氰酸荧光素标记的牛血清白蛋白对单层心脏微血管内皮细胞的穿透能力，以评价apelin对微血管内皮细胞通透性的影响。体内结果表明，在结扎左冠状动脉前降支后，apelin 增加±LV dp/dtmax 和 LVESP 值，降低 LVEDP 值（allp<0.05），并促进大鼠心脏血管生成。体外结果表明，apelin 剂量依赖性地增强增殖、迁移、趋化性和管形成，但不增强心脏微血管内皮细胞的通透性。 Apelin 还增加了心脏微血管内皮细胞中血管内皮生长因子受体 2 (VEGFR2) 和内皮特异性受体酪氨酸激酶 (Tie-2) 的表达。这些结果表明apelin通过上调心脏微血管内皮细胞中VEGFR2和Tie-2的表达来促进血管生成并降低微血管内皮细胞的通透性，从而在心肌梗死中发挥保护作用。
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 (allp< 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.
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影响因子：
20.1
作者：
Frangogiannis NG
通讯作者：
Frangogiannis NG
影响因子：
2.1
作者：
Iribarren C;Phelps BH;Darbinian JA;McCluskey ER;Quesenberry CP;Hytopoulos E;Vogelman JH;Orentreich N
通讯作者：
Orentreich N
影响因子：
7.3
作者：
N. Ward;D. Dumont
通讯作者：
N. Ward;D. Dumont
DOI：
10.1006/bbrc.1998.9489
发表时间：
1998-10-20
影响因子：
3.1
作者：
Tatemoto, K;Hosoya, M;Fujino, M
通讯作者：
Fujino, M
影响因子：
64.5
作者：
Suri, C;Jones, PF;Yancopoulos, GD
通讯作者：
Yancopoulos, GD