miR-410 suppresses the expression of interleukin-6 as well as renal fibrosis in the pathogenesis of lupus nephritis

    loading  Checking for direct PDF access through Ovid


Lupus nephritis (LN) is a highly complex autoimmune disease caused by systemic lupus erythematosus (SLE). MicroRNAs (miRNAs) play a vital role in the pathogenesis of SLE. Previously, a total of 29 miRNAs were identified to be down-regulated in SLE patients, in which miR-410 was likely to be involved in the signalling transduction pathways in regulating the pathogenesis of SLE. The purpose of this study was to investigate the role of miR-410 in LN and to find out whether miR-410 regulates the expression of interleukin (IL)-6 and fibrosis in LN. It was found that the expression level of miR-410 in kidney tissue of MRL/lpr mice was decreased compared to that in BALB/C mice, whereas the level of IL-6 was overexpressed in MRL/lpr mice. Luciferase assay showed that miR-410 binds directly to the 3′ untranslated region (UTR) of IL-6, with the results showing that overexpression of miR-410 significantly decreased the expression level of IL-6 in SV40MES13 cells. Moreover, overexpression of miR-410 significantly reduced the expression levels of fibrosis factors such as transforming growth factor-β1 (TGF-β1) and collagen I/III in SV40MES13 cells; Inhibition of the expression of miR-410 with miR-410 inhibitor resulted in increased levels of IL-6 as well as fibrosis factors. The results identify that miR-410, as a novel and critical factor in the pathogenesis of LN, decreases IL-6 expression by binding directly to the 3′UTR and suppresses fibrosis through down-regulation of TGF-β1 in SV40MES13 cells. Our study brings new insight into understanding the complex mechanisms involved in the pathogenesis of lupus disease.

Related Topics

    loading  Loading Related Articles