The Expression And Mechanism Of MicroRNA-142-3p In Rheumatoid Arthritis

Background Rheumatoid arthritis is a kind of autoimmune diseases characterized by multiple joints involved, synovial inflammation, bone and cartilage destruction, etc. The incidence of adults worldwide is about 0.5% to 1%, which is a major cause of the loss of labor.With persistent and recurrent synovial inflammation and serious joint damage,some even leading to disability, the quality of life with patients suffering from RA is severely reduced. A large number of macrophages accumulate in synovial and cartilage- pannus, which can promote persistent inflammation and joint damage, thus play an extremely important role in the development of rheumatoid arthritis.Macrophages might be activated by some cytokines or cell-to-cell contact. Once activated, macrophages can produce a variety of cytokines and chemokines, such as IL-1 beta, TNF alpha, IL-8 and monocyte chemotactic protein 1(MCP-1). Cytokines interaction may further the progress of chronic inflammation. The etiology and pathogenesis of RA is still unknown. Studies have shown that pathogenesis of RA has significant relationship with abnormal epigenetic regulation. Recently a large number of mi RNA research data suggest it may play an important role in rheumatoid arthritis.Mi RNA can regulate gene expression through post-transcription progression thus participate in various biological processes, which has attracted widespread attention in recent years. Our research detect the expression of mi R-142-3p in patients with RA,as wel as in THP-1 cell, to investigate the effect of mi R-142-3p on the expression of cytokines.Objective To examine expression changes of mi R-142-3p in patients with rheumatoid arthritis and clarify its effect on inflammatory cytokines.Methods1. Mi R-142-3p expression in peripheral blood mononuclear cells with RA patients was detected by stem-loop reverse transcription quantitative real time polybrerase chain reaction and and its correlation with clinical indicators was analyzed.2. PMA was used to induce THP-1 cells. After stimulation of LPS, expression of mi R-142-3p was detected.3. Mi R-142-3p inhibitor was transfected into macrophages and the expression of mi R-142-3p was detected.4. After transfection of mi R-142-3p inhibitor, IL-1 beta, TNF-alpha, IL-8 levels was detected by enzyme linked immunosorbent assay(ELISA) followed the stimulation of LPS.Results1. Compared to osteoarthritis patients and healthy controls, expression level of mi R-142-3p in peripheral blood mononuclear cells of patients with rheumatoid arthritis was higher(P<0.05), and correlated positively with rheumatoid factor(r=0.646, P<0.01).2. After LPS stimulation, the expression of mi R-142-3p in THP-1 macrophages is significantly higher than control(P<0.001).3. After transfection of mi R-142-3p inhibitor into THP-1 macrophages, the relative expression of mi R-142-3p was significantly lower in mi R-142-3p inhibitor transfection group than control(P<0.001).4. The expression of IL-1 beta, TNF-alpha, and IL-8 in cell culture supernatant were decreased significantly after the inhibition of mi R-142-3p(P<0.05).Conclusion1. Mi R-142-3p was upregulated in peripheral blood mononuclear cells with RA patients, and positively correlated with RF, suggesting that mi R-142-3p may be involved in the pathogenesis of RA.2. Inhibiting the expression of mi R-142-3p can restrain the production of inflammatory cytokines, thus targeting mi R-142-3p may have certain effect on inflammation.