Mechanisms of hypoxia-induced transformation in endothelial cells

mct诱导的肺动脉显示了吡莫硝唑的结合，吡莫硝唑是一种缺氧检测剂，可以结合血管壁周围的缺氧区域，包括肺上皮细胞。与对照组相比，Hif-1β+/-小鼠的PAH指数明显减轻，如下数据：左、右室间隔重量比明显降低；肺动脉数目明显增多；内侧厚度指标明显降低。与对照组小鼠相比，mct处理的Hif-1β+/-小鼠的肺动脉肌肉化数量显著减少。此外，有趣的是，给药波生坦（一种内皮素受体阻滞剂）可以将野生型小鼠的PAH改善到与Hif-1β+/-小鼠相同的水平。这些结果表明，内皮细胞中hif -1β介导了mct诱导的PAH的发生。

MCT-induced pulmonary arteries demonstrated binding of pimonidazole, a hypoxia detection agent that binds to regions of hypoxia in the region around vascular walls including lung epithelial cells. Indices of the PAH were significantly alleviated in the Hif-1β+/-mice compared to the control as the following data showed ; the weight ratio of right ventricular to left ventricular with septum was significantly decreased ; the number of pulmonary arteries was significantly increased ; indices of the medial thickness was significantly decreased. The number of musculized pulmonary arteries in MCT-treated Hif-1β+/-mice was significantly decreased compared to that of the control mice. In addition, interestingly, the PAH in wild type mice was ameliorated by administration of bosentan, an endothelin receptor blocker, to the same level of that in Hif-1β+/-mice. These results indicate that the development of MCT-induced PAH was mediated by HIF-1βin endothelial cells.