论文部分内容阅读
目的:探索Lnc01287/miR-4500通过转化生长因子β(TGF-β)/Smad通路影响特发性肺纤维化进展的相关机制。方法:首先原代培养人肺成纤维细胞与人肺瘢痕成纤维细胞，检测Lnc01287、miR-4500、TGF-β/Smad通路在2种细胞中的表达；再通过在线生物信息学网站与双荧光素酶报告基因实验，研究Lnc01287、miR-4500、TGF-β/Smad通路间的相互作用关系；最后通过基因过表达与抑制技术，研究Lnc01287/miR-4500通过TGF-β/Smad通路对人肺瘢痕成纤维细胞增殖的调控。结果:在人肺瘢痕成纤维细胞中，Lnc01287、TGF-β/Smad通路是高表达的，而miR-4500是低表达的。Lnc01287通过靶向抑制miR-4500，然后被抑制的miR-4500通过靶向激活TGF-β/Smad通路，最终促进人肺瘢痕成纤维细胞的生长。结论:Lnc01287是治疗特发性肺纤维化的有希望的靶点，可针对此靶点开发药物，减缓特发性肺纤维化的进展。“,”Objective:To explore related mechanisms of effect of Lnc01287/miR-4500 on the progression of idiopathic pulmonary fibrosis via transforming growth factor-β (TGF-β)/Smad signaling.Methods:Firstly, primary human lung fibroblasts and primary human lung hypertrophic scar fibroblasts were cultured, the expressions of Lnc01287, miR-4500, and TGF-β/Smad signaling between these two cells were compared.Secondly, the relationship among Lnc01287, miR-4500, and TGF-β/Smad signaling was studied via online bioinformatics websites and dual-luciferase reporter assay.Thirdly, how Lnc01287/miR-4500 affects the proliferation of primary human lung hypertrophic scar fibroblasts via TGF-β/Smad signaling was studied by using gene overexpression and suppression techniques.Results:Lnc01287 and TGF-β/Smad signaling were upregulated and miR-4500 was downregulated in primary human lung hypertrophic scar fibroblasts.Lnc01287 targeted miR-4500 to inhibit its expression, then miR-4500 suppression targeted TGF-β/Smad signaling to activate it, and finally the proliferation of primary human lung hypertrophic scar fibroblasts was promoted.Conclusions:Lnc01287 is a promising target to treat idiopathic pulmonary fibrosis.The new drugs that target this molecule can be developed and slow the progression of this disease.