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血管生成素-2通过膜突蛋白介导内皮细胞通透性增高

袁双双 余琴 邓鑫 游婧璨 李永杰 陈妮 王立群

西南医科大学学报2024,Vol.47Issue(3):210-214,5.
西南医科大学学报2024,Vol.47Issue(3):210-214,5.DOI:10.3969/j.issn.2096-3351.2024.03.006

血管生成素-2通过膜突蛋白介导内皮细胞通透性增高

Angiopoietin-2 increases endothelial cell permeability through moesin mediation

袁双双 1余琴 1邓鑫 2游婧璨 2李永杰 2陈妮 2王立群2

作者信息

  • 1. 西南医科大学 代谢性心血管疾病医药基础研究创新中心(泸州 646000)||西南医科大学 心血管药理系(泸州 646000)
  • 2. 西南医科大学 代谢性心血管疾病医药基础研究创新中心(泸州 646000)
  • 折叠

摘要

Abstract

Objective To probe into the functions of angiopoietin-2(Ang-2)in endothelial cell permeability and the potential molecular mechanisms involved.Methods The endothelial cells were plated onto transwell,followed by stimulation with Ang-2(200 ng/mL)and then the endothelial cell permeability were detected.The endothelial cells cultured in 6-well plates were stimulated with Ang-2(200 ng/mL)for 0,15,30 and 60 min.Then the moesin phosphorylation was detected by western blotting.Moreover,the moesin siRNA was used to knock down the expression of moesin and the effects of moesin knockdown on Ang-2-regulated endothelial cell per-meability,stress fiber formation and vascular endothelial cadherin(VE-cadherin)were detected.Results Ang-2 significantly in-creased endothelial cell permeability in a time-dependent manner.The activation of moesin was remarkably evoked with Ang-2 treat-ment for 15 min and peaked in 30 min.However,the anti-Tie-2 antibody significantly prevented Ang-2-induced moesin phosphoryla-tion.Furthermore,knockdown of moesin with moesin siRNA significantly prevented Ang-2-induced endothelial cell permeability in-crease,stress fiber formation and VE-cadherin disruption.Conclusion Ang-2 increased endothelial cell permeability through moesin mediation.

关键词

血管生成素-2/膜突蛋白/内皮细胞通透性

Key words

Angiopoietin-2/Moesin/Endothelial cell permeability

分类

医药卫生

引用本文复制引用

袁双双,余琴,邓鑫,游婧璨,李永杰,陈妮,王立群..血管生成素-2通过膜突蛋白介导内皮细胞通透性增高[J].西南医科大学学报,2024,47(3):210-214,5.

基金项目

国家自然科学基金(81970260) (81970260)

四川省自然科学基金项目(2022NSFSC0671) (2022NSFSC0671)

西南医科大学学报

2096-3351

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