Journal of Capital Medical University ›› 2009, Vol. 30 ›› Issue (2): 161-166.

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Endothelin-1 Promotes Human Pulmonary Artery Smooth Muscle Cells Proliferation by Up-regulation of Capacitative Ca2+ Entry

WANG Cong1,2,3, WANG Chen1,3, WANG Yue-xiu1,2,3, LIU Jie2,3, LI Ji-feng1,2,3, WANG Jun2,3   

  1. 1. Department of Respiratory Diseases, Beijing Chaoyang Hospital, Capital Medical University, Beijing Institute of Respiratory Medicine;2. Department of Physiology, School of Basic Medical Sciences, Capital Medical University;3. Department of Respirology, Capital Medical University
  • Received:2009-01-18 Revised:1900-01-01 Online:2009-04-21 Published:2009-04-21

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Abstract:

Objective This study is designed to investigate the possible signal transduction pathways that related the effect of endothelin-1(ET-1) on HPASMCs proliferation, namely, its effect on the Ca2+ signal pathway. Methods The cultured HPASMCs were divided into following two groups: the control group cultured with smooth muscle basal media (SMBM); the endothelin-1(ET-1) groups incubated with SMBM and ET-1(0.01~1 μmol/L, for 72 h). Cell number was determined with a hemocytometer. MTT assay was used to exam cell viability. ［Ca2+］i was measured by calcium image. Real Time-PCR was performed to detect the expression of TRPC1 gene. Results The cell viability, cell number, CCE, and TRPC1 mRNA transcription were significantly higher after treatment of ET-1. Conclusion ET-1 induced HPASMCs proliferation via up-regulation of TRP channels expression, CCE and ［Ca2+］i.

Key words: store-operated channels, transient receptor potential channels, pulmonary artery smooth muscle cells, pulmonary artery hypertension

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