miR-27a-3p inhibits pulmonary fibrosis by blocking Wnt3a/β-catenin pathway in rats

Objective To observe the effect of miR-27a-3p on bleomycin A5-induced pulmonary fibrosis (PF) in rats and explore the underlying mechanism. Methods Forty-five male SD rats were randomly divided into control group, miR-27a-3p agomir group and miR-27a-3p antagomir group. Each group contained 15 animals. All rats were injected intratracheally with bleomycin A5 to establish PF models. On the first day after bleomycin A5 administration, the rats in the control group, miR-27a-3p agomir group and miR-27a-3p antagomir group were injected at the caudal vein with physiological saline, agomir and antagomir, respectively. Injection was given one time each three days, totally nine times. On day 28, blood samples were collected and then underwent enzyme linked immunosorbent assay for procollagen type 1 carboxyterminal propeptide (P1CP) and procollagen type 3 aminoterminal propeptide (P3NP) concentrations. Subsequently, all rats were sacrificed to remove pulmonary tissue. Both HE and Masson staining were performed to evaluate the pathological changes of PF. The expression of miR-27a-3p, collagen type 1 (Col1), and collagen type 3 (Col3) were detected using fluorescence real time quantitative PCR. Western blotting was used to examine Col1, Col3, Wnt3a and β-catenin levels. Results The miR-27a-3p agomir markedly increased miR-27a-3p expression in the pulmonary tissue, whereas its antagomir decreased it, showing higher transfection efficacy. The pulmonary inflammation and fibrosis degree was alleviated in the miR-27a-3p agomir group while aggravated in the miR-27a-3p antagomir group. In comparison with control group, serum P1CP and P3NP levels decreased in the miR-27a-3p agomir group but increased in the miR-27a-3p antagomir group. Treatment with miR-27a-3p agomir down-regulated the expression of Col1, Col3, Wnt3a and β-catenin in the pulmonary tissue, while miR-27a-3p antagomir up-regulated their expression. Conclusion The miR-27a-3p inhibits the Wnt3a/β-catenin signaling pathway, leading to the down-regulation of Col1 and Col3 expression and the subsequent alleviation of PF.