[Endothelin-1 overexpression inhibits rat pulmonary arterial microvascular smooth muscle cell apoptosis via Akt/PKB pathway]

Zhonghua Xin Xue Guan Bing Za Zhi. 2008 Jun;36(6):551-5.
[Article in Chinese]

Abstract

Objective: To investigate the effects of endothelin-1 (ET-1) overexpression on apoptosis of the rat pulmonary arterial microvascular smooth muscle cells (RPMC) in vitro.

Methods: Primary RPMC obtained from the pulmonary artery and lung microvasculature were identified by immunofluorescence 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 ET(A) expression was significantly higher than that of ET(B) receptor in primary RPMC. Flow cytometry analysis revealed significantly reduced apoptosis in ET-1 transfected RPMC compared to that in vehicle transfected RPMC. Overexpression 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.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Arteries / metabolism
  • Cells, Cultured
  • Endothelin-1 / metabolism*
  • Female
  • Male
  • Muscle, Smooth, Vascular / cytology*
  • Muscle, Smooth, Vascular / metabolism*
  • Proto-Oncogene Proteins c-akt / metabolism
  • Pulmonary Artery / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction

Substances

  • Endothelin-1
  • Proto-Oncogene Proteins c-akt