MiRNA‐199a‐5p positively regulated RANKL‐induced osteoclast differentiation by target Mafb protein

MicroRNAs are involved in osteoclast differentiation. Although miR‐199a‐5p plays an important role in many different systems and diseases, its function during osteoclastogenesis remains unclear. In this study, we investigated the function and the target gene of miR‐199a‐5p in osteoclast differentiation. The in vitro data showed that miR‐199a‐5p was significantly upregulated after the stimulation by receptor activator of nuclear factor kappa‐B ligand in macrophages and RAW 264.7 cells. After transfection of miR‐199a‐5p mimic, the messenger RNA expression level of nuclear factor of activated T‐cells cytoplasmic 1, tartrate‐resistant acid phosphatase (TRAP), and receptor activator of nuclear factor kappa‐B was significantly increased in RAW 264.7 cells and the number of TRAP‐positive cells was also increased. MiR‐199a‐5p inhibitor showed the complete opposite outcome which brought additional proof to our finding. Overexpression of miR‐199a‐5p led to downregulation of Mafb protein. The luciferase activity was obviously repressed when WT‐pGL3‐Mafb and miR‐199a‐5p mimics were cotransfected into 293 T cells and the inhibitors cotransfected demonstrated reverse result. MiR‐199a‐5p overexpressed during osteoclast differentiation and positively regulated osteoclast formation in vitro by target Mafb. Mir‐199a‐5p positively regulated receptor activator of nuclear factor kappa‐B ligand (RANKL)‐induced osteoclast.