Feng X D, Cai Y N
Department of Physiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing.
Sheng Li Xue Bao. 1995 Oct;47(5):448-52.
Hypoxic pulmonary hypertension is characterized by remodeling of pulmonary artery, proliferation and migration of pulmonary artery smooth muscle cells (PASMC), the mechanism of which was studied by observing the effect of hypoxia on DNA synthesis, cell cycle phase and transcription of heat shock protein 70 (HSP70). Our results indicate that hypoxia increases DNA synthesis, enhances the mitogenic effect of ET-1 on PASMC, stimulates quiescent PASMC entering S phase from G0/G1 phase and up-regulates the mRNA level of HSP70. Heat shock proteins are conservative and important stress proteins rendering the cells more tolerable to dangerous stresses by promoting growth and survival of the cells. All these findings suggest that heat shock proteins might also be important to the proliferation of PASMC induced by hypoxia and relevant to the study of the mechanism of hypoxic vascular remodeling.
缺氧性肺动脉高压的特征是肺动脉重塑、肺动脉平滑肌细胞(PASMC)增殖和迁移,通过观察缺氧对DNA合成、细胞周期阶段和热休克蛋白70(HSP70)转录的影响来研究其机制。我们的结果表明,缺氧增加DNA合成,增强ET-1对PASMC的促有丝分裂作用,刺激静止的PASMC从G0/G1期进入S期,并上调HSP70的mRNA水平。热休克蛋白是保守且重要的应激蛋白,通过促进细胞生长和存活使细胞更能耐受危险应激。所有这些发现表明,热休克蛋白可能对缺氧诱导的PASMC增殖也很重要,并且与缺氧性血管重塑机制的研究相关。