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miR‐410 suppresses the expression of interleukin‐6 as well as renal fibrosis in the pathogenesis of lupus nephritis
Author(s) -
Liu Dongmei,
Zhang Na,
Zhang Jing,
Zhao Haiyan,
Wang Xiaofei
Publication year - 2016
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12576
Subject(s) - pathogenesis , lupus nephritis , microrna , transforming growth factor , fibrosis , three prime untranslated region , nephritis , kidney , immunology , interleukin , untranslated region , biology , medicine , cancer research , endocrinology , cytokine , messenger rna , gene , disease , genetics
Lupus nephritis ( LN ) is a highly complex autoimmune disease caused by systemic lupus erythematosus ( SLE ). Micro RNA s (mi RNA s) play a vital role in the pathogenesis of SLE . Previously, a total of 29 mi RNA s 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 SV 40 MES 13 cells. Moreover, overexpression of miR‐410 significantly reduced the expression levels of fibrosis factors such as transforming growth factor‐ β 1 ( TGF ‐ β 1) and collagen I/ III in SV 40 MES 13 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 ‐ β 1 in SV 40 MES 13 cells. Our study brings new insight into understanding the complex mechanisms involved in the pathogenesis of lupus disease.