探地雷达
血管平滑肌
下调和上调
免疫印迹
依普利酮
细胞生长
细胞迁移
化学
内科学
内分泌学
细胞
细胞生物学
雌激素受体
生物
受体
盐皮质激素受体
医学
生物化学
癌症
基因
乳腺癌
平滑肌
作者
Dandan Wang,Minglei Wang,Pingping Sun,Qiaoyan Gao
出处
期刊:Advances in Clinical and Experimental Medicine
[Wroclaw Medical University]
日期:2021-04-29
卷期号:30 (4): 405-412
被引量:3
摘要
Background.Excessive proliferation and migration of vascular smooth muscle cells (VSMCs) are associated with the pathogenesis of atherosclerosis (AS).Eplerenone (EPL), a novel selective aldosterone receptor blocker, plays a substantial role in the treatment of cardiovascular disease.The G protein-coupled estrogen receptor (GPER) is a target of EPL as the STITCH website predicated.Objectives.We aimed to investigate the roles of EPL in AS and identify its potential mechanisms of action. Materials and methods.Oxidized low-density lipoprotein (ox-LDL) was employed to stimulate VSMCs to establish a cellular model of AS.The ability of cell proliferation was examined using a Cell Counting Kit-8, and the expression of proliferation-related proteins was tested using immunofluorescence staining and western blot analysis.Subsequently, cell migration and the expression of migration-associated proteins were evaluated with a wound healing assay, transwell assay and western blot analysis.Then, GPER expression was determined using western blot analysis in the absence or presence of EPL.To explore the regulatory mechanisms of EPL in ox-LDL-stimulated VSMCs, GPER was overexpressed, followed by measurement of cell proliferation and migration.Results.The Ox-LDL stimulation notably upregulated GPER expression, whereas EPL treatment downregulated GPER expression in a dose-dependent manner.Additionally, EPL markedly inhibited proliferation and migration of VSMCs, and the highest dose of EPL resulted in the most marked effect.By contrast, GPER overexpression reversed the inhibitory effects of EPL on proliferation and migration of VSMCs.Conclusions.Eplerenone suppressed ox-LDL-induced proliferation and migration of VSMCs partly through downregulation of GPER, providing a new mechanism of support for EPL use in the clinical treatment of AS.
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