Endothelin-1 overexpression inhibits rat pulmonary arterial microvascular smooth muscle cell apoptosis via Akt/PKB pathway
10.3321/j.issn:0253-3758.2008.06.018
- VernacularTitle:内皮素1过表达经Akt/PKB信号通路抑制大鼠肺细小动脉平滑肌细胞凋亡的体外研究
- Author:
Hai-Qiong HUANG
1
;
Zhen WANG
;
Zhen JIANG
;
Hao-Zhu CHEN
Author Information
1. 复旦大学附属中山医院
- Keywords:
Hypertension,pulmonary;
Myocytes,smooth muscle;
Endothelin-1;
Apoptosis
- From:
Chinese Journal of Cardiology
2008;36(6):551-555
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of endothelin-1 (ET-1) overexpression on apoptosis of the rat pulmonary arterial microvascular smooth muscle celIs(RPMC)in vitro.Methods Primary RPMC obmined from the pulmonary artery and lung microvasculature were identified by imlnanofluorescence staining and electron microscope technique.The RPMC Was transient transfected with the pMEXneo-ET1 and pCDNA5-FRT-TO-ET1-3'UTR plasmids as well as the empty vector respectively via lipofectamine.Flow cytometry was used to assess the cell cycle and apoptosis of RPMC.Akt and Caspase-3 expressions were detected by Western blot and real time RT-PCR.Results The mRNA of ETA expression Was significantly hisher than that of ETB receptor in primary RPMC.Flow cytometry analysis revealed significanflv reduced apoptosis in ET-1 transfected RPMC compared to that in vehicle transfected RPMC.Orerexpression of ET-1 in RPMC also significantly increased the phosphorylation of Akt and reduced the cleaved Caspase-3 expression.Conclusions Overexpression of the ET-1 inhibited RPMC apoptosis and activated Akt/PKB-Caspase-3 signaling pathway,which might be responsible for ET-1 induced the pulmonary microvascular arteries remodeling.
