miR-125a-3p decreases levels of interlukin-17 and suppresses renal fibrosis via down-regulating TGF-β1 in systemic lupus erythematosus mediated Lupus nephritic mice.

Lupus nephritis (LN) is an autoimmune disorder mediated by systemic lupus erythematosus (SLE). Micro RNAs also called as miRs act potentially in the development and progression of SLE. MiR-125a-3p is reported to be down-regulated inpatients of SLE. Aim of the study was to evaluate the function of miR-125a-3p and its effect on regulation of fibrosis and interleukin (IL)-17 in LN. The Renal physiology in MRL/MPJ-Fas lpr/J mice was done by Hematoxylin and eosin staining; expression of miR-125a-3p in renal tissues by RT-PCR, Immunoblotting analysis was done expression of proteins. For in vitro studies, rat mesangial SV40MES13 cells were used and were transfected with vectors. Luciferase activity was done for studying the potential binding of miR-125a-3p with IL-17. It was found that, the expression of miR-125a-3p in kidney tissues of experimental mice were towards lower side versus the control; on the contrary the levels of IL-17 were up-regulated in experimental mice. Luciferase activity suggested that miR-125a-3p binds potentially on the 3'UTR region of IL-17. The assay also suggested up-regulation of miR-125a-3p and suppressed levels of IL-17 in SV40MES13 cells. The up-regulation of miR-125a-3p suppressed the levels of collagen I/II and transforming growth factor-β1 (TGF-β1) in SV40MES13 cells. MiR-125a-3p could be a important factor in the pathogenesis of LN which causes decrease in expression of IL-17 by potentially binding to the 3'UTR region causing suppression of fibrosis via down-regulating TGF-β1 in the SV40MES13 rat mesangial cells.