Effect of high glucose and anoxia on Amot expression in vascular endothelial cells with regard to its function in promoting angiogenesis
10.3760/cma.j.issn.1000-6699.2014.05.016
- VernacularTitle:高糖和缺氧对血管内皮细胞Amot表达的影响及其促血管新生功能研究
- Author:
Yuejie CHU
;
Penghua WANG
;
Daiqing LI
;
Demin YU
- Publication Type:Journal Article
- Keywords:
Amot;
Vascular endothelial cells;
High glucose;
Anoxia;
Angiogenesis
- From:
Chinese Journal of Endocrinology and Metabolism
2014;30(5):428-431
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effects of high glucose and anoxia on Amot expression in vascular endothelial cells (VECs),and explore its role in angiogenesis.Methods VECs were incubated with different glucose concentrations for 48 h,and then cultured at normal oxygen concentration or anaerobic condition for 24 h.The protein expressions of p130-Amot and p80-Amot were detected by Western blot.After Amot expression was downregulated in VECs by siRNA,wound healing experiments and angiogenesis experiments were performed to test the effect of decreased Amot expression on angiogenesis.Results pl30-Amot protein expressions in low glucose (5.5mmol/L) plus normal oxygen group and low glucose plus anaerobic group were higher than those in high glucose (30mmol/L) plus normal oxygen group,high glucose plus anaerobic group,middle glucose (15 mmol/L) plus normal oxygen group,and middle glucose plus anaerobic group (all P＜0.01).Compared with low glucose plus anaerobic group,p130-Amot expression was higher in low glucose plus normal oxygen group (P ＜ 0.01).However,the expression of p80-Amot showed no statistically significant difference among different groups (P＞0.05).Compared to the normal VECs,the cells with decreased Amot expression by siRNA exhibited an attenuated cell migration in the wound healing experiments and a lesser tube formation in the angiogenesis experiments.Conclusions High glucose exerts a more significantly negtive effect on the Amot expression than anoxia in VECs.The downregulation of Amot expression inhibits migration and angiogenesis of VECs.
