MicroRNA-155 inhibitor ameliorates collagen-inducedarthritis by modulating the phenotype of pro-inflammatorymacrophages in a mouse model

Abstract

 Background: Here, we aimed to illustrate the roles of microRNA (miR)-155 in collagen-induced arthritis (CIA) and its underlying mechanisms.Methods: A mouse model of CIA was first established, and miR-155 inhibitor was intravenously injected.In in vitro studies, bone marrow-derived macrophages (BMDMs) were induced to M1 macrophages followed by the treatment of miR-155 inhibitor. RT-qPCR was applied to determine the mRNA expression.The frequency of M1 or M2 macrophages was determined by flow cytometry. Western blotting was employed to detect protein expression. Enzyme-linked immunosorbent assay was employed to measure the production of inflammatory cytokines and anti-collagen antibody.Results: The levels of miR-155 were increased in macrophages from rheumatoid arthritis (RA) patients and M1 macrophages. The treatment of miR-155 inhibitor decreased inflammatory cytokines in M1 macrophages. Besides, treatment of miR-155 inhibitors promoted the differentiation of M0 macrophages into M2 macrophages. In vivo studies showed that miR-155 inhibitors ameliorated the RA symptoms by decreasing inflammatory cytokines in the CIA mouse model. Treatment of miR-155 also led to decreased M1 macrophage biomarker and increased M2 macrophage biomarker.Conclusion: MiR-155 inhibitor ameliorates RA symptoms in part by regulating macrophage phenotypes.