Pulmonary arterial hypertension (PAH), also known as broilers ascites syndrome, is characterized by hypoxia, pulmonary artery pressure, and right heart failure. However, less information is available about the molecular mechanisms of PAH. We evaluated the mediation of calcium-sensing receptor by inducing hypoxia for the possible proliferation of pulmonary artery smooth muscle cells via the G protein pathway. For this purpose, we used an in vitro trial of chicken cell culture and confirmed our results by using immunohistochemistry, immunofluorescence staining, quantitative real-time polymerase chain reaction assay, and Western blotting analysis. Our results showed that the mRNA and protein expression levels of calcium-sensing receptor (CaSR) were significantly upregulated in cells when co-incubated with CaCl2. However, the levels of mRNA and protein were obviously decreased when supplemented with blocking agents (NiCl2, 2-APB, and D609). Furthermore, the experimentally induced hypoxia also upregulated the expression of CaSR gene as compared to CaSR gene expression in control cells. Together, these results indicate that hypoxia plays an important role in the expression of CaSR gene in pulmonary artery smooth muscle cells and reveals new targets for the CaSR excited hypothesis to prevent and control PAH in chickens.

中文翻译：

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钙敏感受体通过G蛋白-PLC-IP3途径仲裁低氧诱导的肺动脉平滑肌细胞增殖。

肺动脉高压（PAH），也称为肉鸡腹水综合征，其特征是缺氧，肺动脉压和右心衰竭。但是，有关PAH分子机制的信息很少。我们通过诱导缺氧，通过G蛋白途径对肺动脉平滑肌细胞的增殖进行了评估，从而评估了钙敏感受体的介导作用。为此，我们使用了鸡细胞培养的体外试验，并通过免疫组织化学，免疫荧光染色，定量实时聚合酶链反应分析和Western印迹分析证实了我们的结果。我们的结果表明，与CaCl2共同孵育时，钙敏感受体（CaSR）的mRNA和蛋白质表达水平显着上调。然而，补充阻断剂（NiCl2、2-APB和D609）后，mRNA和蛋白质水平明显降低。此外，与对照细胞中的CaSR基因表达相比，实验诱导的缺氧还上调了CaSR基因的表达。总之，这些结果表明缺氧在肺动脉平滑肌细胞中CaSR基因的表达中起着重要作用，并揭示了CaSR兴奋假说预防和控制鸡PAH的新靶标。