Author + information
- Yang Zhiming,
- Jingjing Xue,
- Huiyu Yang,
- Bin Liang,
- Yanan Zhao and
- Zhiming Yang
To investigate the protective effect of Ang 1-7 against ox-LDL -induced endoplasmic reticulum stress(ERS) and apoptosis via Mas Receptor in Human umbilical vein endothelial cells(HUVECs),and provide a potential therapeutic strategy that the Ang 1-7/Mas receptor axis to treat ox-LDL-induced cardiovascular diseases related to ER stress.
HUVECs were cultured in 1640 medium containing 12% fetal bovine serum,1% penicillin and streptomycin. After 50% confluence was obtained, they were treated medium without FBS for 12 h, and later were replaced with new complete media, Experiment was divided into five groups: the control group; the ox-LDL group:cells were exposed to ox-LDL (75mg/L) 30 min; the Ang-(1-7)+ ox-LDL group: cells were exposed to Ang-(1-7) (1000nmol/L) 30 min before exposure to ox-LDL (75mg/L) for 24 h; the A-779 +Ang-(1-7)+ ox-LDL group: cells were exposed to A-779 (1000nmol/L) 30 min before exposure to Ang-(1-7) (1000nmol/L) for 30 min,and after 1h were replaced with ox-LDL (75mg/L) for 24 h. the A-779 + ox-LDL group: cells were exposed to A-779 (1000nmol/L) 30 min before exposure to ox-LDL (75mg/L) for 24 h. We performed the following experimental procedures: RT-qPCR, caspase-3,Tunel and Western blot analysis.
The expression of ER stress proteins were elevated by ox-LDL in HUVECs. This elevation was reversed by co-incubation with Ang 1-7 while the presence of A779 antagonized the effect of Ang 1-7. Ox-LDL-induced increase in the mRNA expression of CHOP and GRP78 (ER chaperones) was also inhibited by Ang 1-7, which was again antagonized by A779. Likewise, ox-LDL -treated HUVECs exhibited an elevated apoptosis, which was blunted by co-treatment with Ang 1-7 and the latter effect was reversed by A779.
Ox-LDL stimulated ER stress contributes to endothelial apoptosis. Ang- (1-7) protects against ox-LDL -Induced Endothelial Endoplasmic Reticulum Stress and apoptosis is most likely mediated via Mas receptor