angiotensin ii mediates the high-glucose-induced endothelial-to-mesenchymal transition in human aortic endothelial cells血管紧张素ⅱ介导high-glucose-induced endothelial-to-mesenchymal转变人类主动脉内皮细胞.pdfVIP

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angiotensin ii mediates the high-glucose-induced endothelial-to-mesenchymal transition in human aortic endothelial cells血管紧张素ⅱ介导high-glucose-induced endothelial-to-mesenchymal转变人类主动脉内皮细胞.pdf

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Tang et al. Cardiovascular Diabetology 2010, 9:31 CARDIO /content/9/1/31 VASCULAR DIABETOLOGY ORIGINAL INVESTIGATION Open Access Angiotensin II mediates the high-glucose-induced endothelial-to-mesenchymal transition in human aortic endothelial cells * Rining Tang, Qing Li, Linli Lv, Houyong Dai, Min Zheng, Kunling Ma, Bicheng Liu Abstract Background: Substantial evidence suggests that high glucose (HG) causes endothelial cell damage; however, the potential mechanism therein has yet to be clarified. The aim of this study was to investigate the influence of HG on the endothelial-to-mesenchymal transition (EndMT) and its relevance to the activation of the renin-angiotensin system. Methods: Primary human aortic endothelial cells (HAECs) were divided into three groups: a normal glucose (NG) group, HG group, and irbesartan (1 μM)-treated (HG+irbesartan) group. The concentration of angiotensin II in the supernatant was detected by radioimmunoassay. Pathological changes were investigated using fluorescence microscopy and electron microscopy. Immunofluorescence staining was performed to detect the co-expression of CD31 and fibroblast markers, such as fibroblast-specific protein 1 (FSP1). The expressions of FSP1 and a-SMA were detected by RT-PCR and Western blot. Results: The treatment of HAECs in the HG group resulted in significant increases in the expressions of FSP1 and angiotensin II in dose-and time-dependent manners. The incubation of HAECs exposure to HG resulted in