miR-146a-5p attenuates IL-1β-induced IL-6 and IL-1β expression in a cementoblast-derived cell line

Objective miR-146a is widely induced during the immune response. However, little is known about the biogenesis, function and mechanism of miR-146a in cementoblasts during the pathogenesis of periodontitis. This study aimed to investigate the effects of miR-146a in murine cementoblast-derived OCCM-30 cells following IL-1 beta stimulation. Materials and methods OCCM-30 cells were cultured and exposed to IL-1 beta. IL-6, IL-1 beta and TNF-alpha, and miR-146a-5p expression was assessed by qRT-PCR. Mimics/inhibitors were transiently transfected into cells to determine the function of miR-146a-5p. Signalling pathways including p38 MAPK, ERK1/2 and NF-kappa B were studied by using specific inhibitors. The indicated proteins were measured by Western blot analysis and ELISA. Results In IL-1 beta-stimulated OCCM-30 cells, the expression levels of miR-146a-5p along with IL-6 and IL-1 beta increased in a time-dependent manner. The ERK1/2, p38 MAPK and NF-kappa B pathway were activated upon IL-1 beta stimulation. Blocking the NF-kappa B pathway decreased IL-6, IL-1 beta and miR-146a-5p expression. The overexpression of miR-146a-5p reduced IL-6 and IL-1 beta expression, while the inhibition of miR-146a-5p increased IL-6 and IL-1 beta expression in IL-1 beta-treated OCCM-30 cells. miR-146a-5p attenuated IL-6 and IL-1 beta expression via the IRAK1/TRAF6 pathway. Conclusion This study suggested that miR-146a-5p attenuates IL-1 beta-induced inflammatory factors in cementoblast-derived cell line.