microRNA-26a对上皮间质转化的作用及分子机制
首发时间:2016-01-19
摘要:目的:研究microRNA-26a (miR-26a)对上皮间质转化(Epithelial Mesenchymal Transition, EMT)的作用,明确miR-26a在特发性肺纤维化发生时的作用及其作用机制。方法:通过气管注射博莱霉素建立小鼠肺纤维化模型。离体实验培养A549细胞系,给予TGF-β1刺激诱导出EMT细胞模型,同时转染miR-26a,Negative Control (NC),验证miR-26a对EMT的调控作用。结果:miR-26a在肺纤维化小鼠中表达降低,miR-26a可以靶向调控高迁移率族蛋白A2(High Mobility Group Protein A2,HMGA2)表达,在A549细胞中,过表达miR-26a可抑制TGF-β1诱导的EMT。结论:miR-26a通过调控HMGA2表达进而逆转EMT,进一步揭示了miR-26a对IPF可能的治疗机制和意义。
关键词: 药理学 特发性肺纤维化 上皮间质转化 microRNA-26a 高迁移率族蛋白A2
For information in English, please click here
The effect and mechanism of microRNA-26a on epithelial-mesenchymal transition
Abstract:Objective: To explore the role and mechanisms of microRNA-26a (miR-26a) on epithelial-mesenchymal transition (EMT). Methods: The pulmonary fibrosis model were established by intratracheally injection of Bleomycin (BLM). A549 cells were treated with TGF-β1 or transfected with miR-26a to examine the effect of miR-26a on EMT. Results: miR-26a was down-regulated in the mice with experimental pulmonary fibrosis. High Mobility Group Protein A2 (HMGA2) is one of the targets of miR-26a. Over-expression of miR-26a attenuated TGF-β1-induced EMT in cultured A549 cells. Conclusion: miR-26a reverses EMT by direct regulation of HMGA2, and which expand the understanding of the mechanism of pulmonary fibrosis.
Keywords: Pharmacology Idiopathic Pulmonary Fibrosis Epithelial-Mesenchymal transition microRNA-26a HMGA2?????
论文图表:
引用
No.4676075110894914****
同行评议
共计0人参与
勘误表
microRNA-26a对上皮间质转化的作用及分子机制
评论
全部评论0/1000