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目的研究miR-214在肺动脉高压发病机制中的调控作用。方法应用逆转录聚合酶链式反应(qRT-PCR)方法检测miR-214在肺动脉高压患者血清及缺氧诱导肺动脉平滑肌细胞中表达;通过EdU渗入法以及划痕实验研究miR-214对肺动脉平滑肌细胞增殖及迁移的影响;对miR-214靶基因预测并验证。结果肺动脉高压患者血清中miR-214显著高于正常人血清(p<0.001);经过缺氧处理肺动脉平滑肌细胞明显促进miR-214表达(p<0.01);miR-214促进缺氧条件下的肺动脉平滑肌细胞增殖、迁移;双荧光素酶报告系统证明miR-214能够与缺氧诱导因子1α抑制因子(HIF1AN)的3’-UTR结合;HIF1AN为miR-214在肺动脉平滑肌细胞中的靶向基因。结论miR-214可能通过靶基因HIF1AN参与肺动脉高压调节机制。
Objective To study the regulatory role of miR-214 in the pathogenesis of pulmonary hypertension. Methods miR-214 was detected by reverse transcriptase-polymerase chain reaction (qRT-PCR) in the serum and hypoxia-induced pulmonary artery smooth muscle cells of patients with pulmonary hypertension. The effects of miR-214 on pulmonary artery smooth muscle cells Proliferation and migration; prediction and verification of miR-214 target gene. Results The serum level of miR-214 in patients with pulmonary hypertension was significantly higher than that in normal people (p <0.001); miR-214 expression was significantly enhanced by hypoxic pulmonary artery smooth muscle cells (p <0.01); miR-214 promoted pulmonary artery hypoxia Smooth muscle cell proliferation and migration. Dual luciferase reporter system proved that miR-214 can bind to 3’-UTR of hypoxia-inducible factor 1α inhibitor (HIF1AN), and HIF1AN is a target gene of miR-214 in pulmonary artery smooth muscle cells. Conclusion miR-214 may be involved in the regulation of pulmonary hypertension by HIF1AN.