中文摘要：

目的 研究经典型瞬时受体电位6（transient receptor potential canonical 6,TRPC6）对大鼠肺动脉平滑肌细胞（rat pulmonary artery smooth muscle cells,RPASMCs）增殖、侵袭和凋亡能力的影响. 方法 以RPASMCs为研究对象,构建TRPC6的siRNA以及过表达载体,转入细胞后采用MTT法、Transwell小室法、流式细胞法观察其对RPASMCs增殖、侵袭及凋亡能力的影响. 结果 增殖实验结果表明TRPC6过表达组可促进RPASMCs增殖,其OD值为1.13 ±0.09,TRPC6-siRNA组则可抑制RPASMCs增殖,其OD值为0.42 ±0.03;细胞侵袭结果表明TRPC6过表达组可促进RPASMCs侵袭,穿膜细胞数为108±7,TRPC6-siRNA组则可抑制RPASMCs侵袭,穿膜细胞数为38 ±3;流式细胞仪检测发现TRPC6对PASMCs凋亡几乎无影响.结论 TRPC6可显著促进RPASMCs的增殖和侵袭,在肺动脉高压的发生和发展中起着重要作用,对进一步研究TRPC6在肺动脉高压中的作用及机制奠定了基础.

英文摘要：

Objective To investigate the effects of transient receptor potential canonical 6 （TRPC6） on the proliferation,invasion and apoptosis of rat pulmonary artery smooth muscle cells（RPASMCs）.Methods The siRNA and overexpression vectors of TRPC6 were constructed,and then transfected into RPASMCs.MTT assay,transwell chamber and flow cytometry were used to determine the effects of TRPC6 on the proliferation,invasion and apoptosis of RPASMCs.Results MTT results showed that the proliferation of RPASMCs was promoted after treated with TRPC6-overexpression （1.13 ± 0.09）,while the pretreatment with TRPC6-siRNA inhibited the proliferation of RPASMCs （0.42 ± 0.03）.Furthermore,the invasion of RPASMCs was significantly promoted by TRPC6-upregulation,while the pretreatment with TRPC6-siRNA inhibited the invasion of RPASMCs,and the number of RPASMCs traveling through the polycarbonate filters was 108 ± 7 and 38 ± 3,respectively.The flow cytometry results demonstrated that TRPC6 had no effect on the apoptosis of RPASMCs.Conclusion TRPC6 could promote the proliferation,invasion of RPASMCs and play an important role in the development of pulmonary artery hypertension,which lay a foundation for studying the role and mechanism of TRPC6 in pulmonary artery hypertension.