microRNA-26a抑制特发性肺纤维化的作用及机制

Objective: To examine the effect of microRNA-26a (miR-26a) in the process of idiopathic pulmonary fibrosis (IPF) and reveal its potential role on clinic. Methods: Real-time PCR was used to detect the expression of miR-26a in IPF patients. Pulmonary fibrosis model in mice were established by intratracheally injection of Bleomycin (BLM). Cultured A549 cells were treated with TGF-β1 or transfected with miR-26a to examine the effect of miR-26a on collagen deposition. Western blot and immunofluorescence were applied to observe the occurrence of epithelial-mesenchymal transition (EMT), and Sircol Collagen Assay Kit was used to detect the content of collagen. Results: miR-26a was decreased in the lung of IPF patient. Forced expresion of miR-26a inhibited the EMT and collagen deposition in BLM-treated mice. Overexpression of miR-26a attenuated TGF-β1 induced production of collagen in A549 cells. Conclusion: miR-26a alleviates collagen deposition both in TGF-β1 treated A549 cells and BLM-treated mice, and then inhibits EMT and lung fibrosis. This study confirmed the anti-fibrotic action of miR-26a and elucidated its mechanism.