LAUSR.org creates dashboard-style pages of related content for over 1.5 million academic articles. Sign Up to like articles & get recommendations!

MicroRNA-183 exerts a protective role in lupus nephritis through blunting the activation of TGF-β/Smad/TLR3 pathway via reducing Tgfbr1.

Photo from wikipedia

PURPOSE The role of microRNA (miR)-183 has been elucidated in systemic lupus erythematosus, while whether it is also engaged in the lupus nephritis (LN) development remains opaque. The intention of… Click to show full abstract

PURPOSE The role of microRNA (miR)-183 has been elucidated in systemic lupus erythematosus, while whether it is also engaged in the lupus nephritis (LN) development remains opaque. The intention of this study is to examine the relevance of miR-183 downregulation in the pathogenesis of LN. METHODS The expression of miR-183 was first detected in MRL/lpr mice at weeks 8 and 12, followed by the assessment the effects of miR-183 on renal fibrosis and inflammatory response after overexpression or silencing of miR-183 in mice with LN. We further overexpressed or knocked-down miR-183 in human renal glomerular endothelial cells (HRGECs), and detected the expression patterns of inflammatory factors and Vimentin and α-SMA in the cells. Differentially expressed genes in HRGECs overexpressing miR-183 by microarrays were intersected with targeting mRNAs of miR-183 predicted by bioinformatics websites. The effects of transforming growth factor beta receptor 1 (Tgfbr1) and TGF-β/Smad/TLR3 pathway on renal damage in mice were verified by rescue experiments. RESULTS miR-183 expression was notably lower in MRL/lpr mice, and increased miR-183 expression inhibited renal fibrosis and inflammatory response in mice with LN. Moreover, miR-183 inhibitor in HRGECs remarkably promoted the expression of Vimentin and α-SMA and the secretion of inflammatory factors. miR-183 protected the mouse kidney from pathological damages by targeting and inhibiting Tgfbr1 expression. CONCLUSION miR-183 inhibited the expression of Tgfbr1 by direct targeting to disrupt the TGF-β/Smad/TLR3 pathway, thus repressing renal fibrosis and the secretion of inflammatory factors in LN.

Keywords: tlr3 pathway; tgf smad; mir 183; expression; smad tlr3; lupus

Journal Title: Experimental cell research
Year Published: 2020

Link to full text (if available)


Share on Social Media:                               Sign Up to like & get
recommendations!

Related content

More Information              News              Social Media              Video              Recommended



                Click one of the above tabs to view related content.