[Endothelin-1 induces chemotaxis of pulmonary artery smooth muscle cells].
Migration of pulmonary artery smooth muscle cells (PASMC) and their precorsors might be an important mechanism of pulmonary vascular structural remodelling associated with hypoxic pulmonary hypertension (HPH). Endothelin-1 (ET-1) plays an important role in the pathogenesis of HPH. This study observed that ET-1 induced chemotaxis of PASMC in a dose dependent manner. The maxium chemotactic response of PASMC to ET-1 occured at a concentration of 10(-9) mol/L. The chemotactic activity of ET-1 is weakened, when its concentration is higher than 10(-9) mol/L. BQ123, a specific antagonist of ETRA, significantly inhibited the chemotaxis of PASMC induced by ET-1, which indicates that the chemotactic activity of ET-1 may be mediated by ETRA. Hypoxia enhanced the chemotaxis of PASMC induced by ET-1. This study suggests that ET-1 and hypoxia might stimulate the migration of PASMC and/or its precorsor. The further mechanism is under study.
Feng
X
X
Institute of Basic Medical Sciences, CAMS, Beijing.
Cai
Y
Y
Dawes
K E
KE
Laurent
G J
GJ
D000818:Animals; D002417:Cattle; D015687:Cell Hypoxia; D002478:Cells, Cultured; D002633:Chemotaxis / Q000187:drug effects*; D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1 / Q000494:pharmacology*; D009131:Muscle, Smooth, Vascular / Q000166:cytology* / Q000502:physiology; D010456:Peptides, Cyclic / Q000494:pharmacology; D011651:Pulmonary Artery / Q000166:cytology
D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1; D010456:Peptides, Cyclic; C072247:cyclo(Trp-Asp-Pro-Val-Leu)