Regulatory mechanisms of miR-212-3p on the secretion of inflammatory factors in monocyte-macrophages and the directed differentiation into osteoclasts in ankylosing spondylitis.

Abstract

To explore the mechanisms of action of micro ribonucleic acid (miR)-212-3p in the secretion of inflammatory factors in monocyte-macrophages and the directed differentiation into osteoclasts (OCs) in ankylosing spondylitis (AS), proteoglycan was used to establish an AS mouse model. The mouse monocyte-macrophages were cultured in vitro, transfected with miR-212-3p mimic, and added with phosphorylated-extracellular signal-regulated kinase (p-ERK)1/2 agonist Ro67-7476 in vitro. After the cells were transfected with the miR-212-3p mimic in each group, the expressions of p-ERK1/2, matrix metalloproteinase-1 (MMP-1), MMP-3, interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) significantly declined, whereas those of tartrate-resistant acid phosphatase (TRAP), calcitonin, and p-nuclear factor of activated T cell 1 (NFATC1) significantly rose. After Ro67-7476 was added, the protein expressions of p-ERK1/2, MMP-1, MMP-3, IL-1β, and TNF-α were significantly increased in each group, but they displayed decreasing trends in cells transfected with the miR-212-3p mimic. In contrast, the protein expressions of TRAP, calcitonin, and p-NFATC1 declined, but they showed increasing trends in cells transfected with the miR-212-3p mimic. miR-212-3p can, through inhibiting the phosphorylation of p-ERK1/2, prevent the aggregation of macrophages and the secretion of inflammatory factors. It also up-regulates the expression of OC marker proteins to facilitate the differentiation and maturation of OCs, ultimately relieving AS-induced inflammation and new bone growth-induced joint neoplasm.