海南医科大学学报2026，Vol.32Issue(8)：561-569,9.DOI:10.13210/j.cnki.jhmu.20250926.001
非肌肉肌球蛋白ⅡA维持高糖诱导的脑微血管内皮细胞功能
Non-muscle myosin ⅡA preserves the functionality of brain microvascular endothelial cells in high glucose environments
摘要
Abstract
Objective:To investigate the mechanism of non-muscle myosin ⅡA(NMⅡA)in high glucose(HG)-induced in-jury of brain microvascular endothelial cells bEnd.3.Methods:An in vitro diabetic cerebrovascular injury model was established by culturing bEnd.3 cells in HG medium.NMⅡA expression was knocked down using siRNA,followed by assessments of cell viabil-ity,inflammatory factors,oxidative stress markers,and cellular morphological changes.Functional assays(CCK-8,wound heal-ing,atomic force microscopy)were performed to evaluate proliferation,migration,invasion,and mechanical properties.Protein and gene expression were analyzed by Western blot and RT-qPCR.Results:The HG-induced bEnd.3 model was successfully es-tablished.NMⅡA knockdown exacerbated inflammation and oxidative stress,reduced cell viability and migration,and decreased cell height,adhesion,and Young's modulus(P<0.05).Conclusion:NMⅡA regulates critical processes including cell contrac-tion,migration,and tension maintenance.Under HG conditions,NMⅡA deficiency worsens inflammation and impairs endotheli-al function,suggesting its pivotal role in preserving cerebrovascular homeostasis(P<0.05).Targeting NMⅡA may offer a novel therapeutic strategy for diabetic cerebrovascular complications.关键词
糖尿病/脑微血管内皮细胞/非肌肉肌球蛋白ⅡA(NMⅡA)/高糖/细胞损伤Key words
Diabetes mellitus/Cerebral microvascular endothelial cells/Non-muscle myosin ⅡA(NMⅡA)/High glucose/Cell injury分类
医药卫生引用本文复制引用
赵玉洁,谭越雯,薛晋垣,周翊栋,曹佳会..非肌肉肌球蛋白ⅡA维持高糖诱导的脑微血管内皮细胞功能[J].海南医科大学学报,2026,32(8):561-569,9.基金项目
This study was supported by the National Natural Science Foundation of China(32000551) 国家自然科学基金(32000551) （32000551）
