[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.