血管紧张素Ⅱ介导高糖诱导的人主动脉内皮细胞转分化  

Angiotesin Ⅱ mediates the high glucose-induced endothelial-to-mesenchymal transition in human aortic endothelial cells

作　　者：汤日宁[1] 戴厚永[1] 李青[1] 吕林莉[1] 张建东[1] 马坤岭[1] 刘必成[1] 

机构地区：[1]东南大学附属中大医院,东南大学肾脏病研究所,南京210009

出　　处：《中国糖尿病杂志》2011年第5期361-365,共5页Chinese Journal of Diabetes

基　　金：国家自然科学基金资助项目(30870953);江苏省自然科学基金重点项目(2007709)

摘　　要：目的探讨高糖对内皮细胞转分化的影响及其与血管紧张素Ⅱ(ATⅡ)的关系。方法将人主动脉内皮细胞分成正常浓度葡萄糖(NG)组、高糖(HG)组和厄贝沙坦干预(HG+Irb)组。放射免疫法检测细胞上清液中ATⅡ的浓度。共聚焦显微镜观察CD31和成纤维细胞特异蛋白1(FSP1)的双染色结果。Western blot检测FSP1蛋白水平的表达。结果与NG组比,高糖刺激的内皮细胞导致ATⅡ和FSP1表达增加(P<0.05),呈浓度和时间依赖性。共聚焦显微镜可见CD31和FSP1表达重叠,且一些细胞获得纺锤样的改变并失去CD31染色。厄贝沙坦可抑制高糖引起的上述改变(P<0.05)。结论高糖可能通过ATⅡ介导的内皮细胞转分化导致内皮细胞损伤,而厄贝沙坦抑制内皮细胞转分化。Objective The aim was to investigate the influence of high glucose on endothelial to mesenchymal transition （EnchMT） and its relevance with the activation of angiotensin Ⅱ. Methods Human aortic endothelial cells （HAEC） were divided into three groups： normal glucose group （NG）, high glucose group （HG） and the Irbesartan （1μmol/L） treated group. The concentration of angiotensin Ⅱ in the HAEC supernatant was detected by radioimmunoassay. Immunofluorescence staining was performed to detect the co-expression of CD31 and fibmblast specific protein1 （FSP1）. Results HG led to a significant increase of expression of angiotensin Ⅱ and FSP1 protein in HAEC in dose and time dependent manner. Double staining of HAEC showed co-localization of CD3l and FSP1. These changes were inhibited by treatment with irbesartan （P〈0. 05）. Conclusion These findings suggest a novel mechanism on the high glucose FIG induced endothelial damage through angiotensin Ⅱ mediated EndMT, which is inhibited by irbesartan.

关 键 词：高糖 内皮细胞转分化 血管紧张素Ⅱ 厄贝沙坦 

分 类 号：R587.2[医药卫生—内分泌]