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目的 探讨低氧对肺动脉平滑肌和内皮细胞蛋白激酶C (PKC)αmRNA表达的影响。方法 应用原位杂交技术观察了大鼠不同节段肺动脉平滑肌细胞和内皮细胞PKCαmRNA的分布及低氧对在体和离体肺动脉平滑肌细胞及内皮细胞PKCαmRNA表达的影响。结果 正常大鼠各级肺动脉平滑肌细胞和内皮细胞均有PKCαmRNA的表达 ,腺泡内肺动脉平滑肌细胞中的表达明显高于肌型肺动脉 (P <0 .0 1) ;低氧 14d和 2 8d肌型动脉和腺泡内肺动脉内皮细胞的表达均明显增高(P <0 0 1) ,腺泡内肺动脉平滑肌细胞的表达较对照组明显升高 (P <0 .0 1) ,低氧 14d肌型肺动脉平滑肌细胞表达升高不明显 ,但低氧 2 8d明显升高 (P <0 .0 1)。正常条件下离体培养猪肺动脉平滑肌细胞和内皮细胞均有PKCαmRNA的表达 ,低氧 1h对其表达无明显影响 ,48、72h表达明显升高 ,以72h升高最显著 (P <0 .0 0 1)。结论 低氧可促进肺动脉平滑肌细胞和内皮细胞PKCαmRNA的表达 ,而以腺泡内肺动脉平滑肌细胞的变化最明显 ,PKCα在低氧性肺动脉高压的形成中可能起一定作用。
Objective To investigate the effect of hypoxia on protein kinase C (PKC) αmRNA expression in pulmonary artery smooth muscle and endothelial cells. Methods The in situ hybridization technique was used to observe the distribution of PKCα mRNA in pulmonary artery smooth muscle cells and endothelial cells of different segments and the effect of hypoxia on PKCα mRNA expression in cultured and isolated pulmonary artery smooth muscle cells and endothelial cells. Results The expression of PKCαmRNA in pulmonary artery smooth muscle cells and endothelial cells at all levels of normal rats was significantly higher than that in muscle pulmonary artery (P <0.01), while that in hypoxia 14d and 28d The expression of pulmonary artery endothelial cells in arteries and acinus were significantly increased (P <0.01), the expression of pulmonary artery smooth muscle cells in acinus was significantly higher than that in control group (P <0.01) Smooth muscle cells increased expression was not obvious, but hypoxia 28d significantly increased (P <0.01). Under normal conditions, the expression of PKCαmRNA in porcine pulmonary artery smooth muscle cells and endothelial cells were all in vitro. The expression of PKCαmRNA was not affected by hypoxia for 1h, and increased significantly at 72h and 72h (P <0.05) 1). Conclusions Hypoxia can promote the expression of PKCαmRNA in pulmonary artery smooth muscle cells and endothelial cells, but the most obvious changes are in the pulmonary artery smooth muscle cells in the acinar cells. PKCα may play a role in the formation of hypoxic pulmonary hypertension.