内皮素－1诱导肺动脉平滑肌细胞的趋化反应

本实验发现ＥＴ－１可诱导肺动脉平滑肌细胞（ＰＡＳＭＣ）的趋化反应，１０~（－１２）～１０~（－９）ｍｏｌ／ＬＥＴ－１可剂量依赖地促进ＰＡＳＭＣ的趋化反应，而高浓度的ＥＴ－１（１０~（－８）～１０~（－６）ｍｏｌ／Ｌ）对ＰＡＳＭＣ的趋化作用减弱，内皮素Ａ型受体的特异拮抗剂ＢＱ１２３可抑制ＰＡＳＭＣ对ＥＴ－１的趋化反应，此外还观察到缺氧可促进ＰＡＳＭＣ对ＥＴ－１的趋化反应。提示ＥＴ－１可能对缺氧性肺血管结构重组中平滑肌细胞及其前体的迁移具有重要作用。

Endothelin-1 Induces Chemotaxis of Pulmonary Artery Smooth Muscle Cells

Migration of pulmonary artery smooth muscle cells(PASMC)and their precorsorsmight be an important mechanism of pulmonary vascular structural remodelling associatedwith hypoxic pulmonary hypertension(HPH).Endothelinl(ET-1)plays an important rolein the pathogenesis of HPH.This study observed that ET-1 induced chemotaxis of PASMCin a dose dependent manner.The maxium chemotactic response of PASMC to ET-1 occuredat a concentration of 10-9mol/L.The chemotactic activitv of ET-1 is weakened,when itsconcentration is higher than 10-9mol/L. BQ123,a specific antagonist of ETRA,significantlyinhibited the chemotaxis of PASMC induced by ET-1, which indicates that the chemotacticactivity of ET-1 may be mediated by ETRA.Hypoxia enhanced the chemotaxis of PASMC in-duced by ET-1.This study suggests that ET-1 and hypoxia might stimulate the migration ofPASMC and/or its precorsor,The further mechanism is under study.