Changes and significance of TLR4/SOCS3/miR-203 expression in renal tissues of rats with IgA nephropathy

XIAO Jun; HU Yan-ping; TU Lu-xia; WEI Xin; CHEN Qin-kai

doi:10.3969/j.issn.1001-9448.2019.05.005

Abstract：Objective To observe the expression of toll-like receptor 4 (TLR4), cytokine signal transduction inhibitor 3 (SOCS3) and miR-203 in renal tissues of IgA nephropathy (IgAN) rat model, and to investigate its role in the pathogenesis of IgAN. Methods The experimental IgAN rat model was established by immune induction method. The kidneys of the rats were harvested at the 8 th and 9 th week of the model setting, and the renal tissue IgA expression was tested by immunofluorescence assay. The degree of glomerular mesangial hyperplasia was evaluated through the high Iodate-Schiff (PAS) staining. The expression of TLR4 and SOCS3 proteins were measured by western blotting, and the expression levels of TLR4 mRNA, SOCS3 mRNA and miR-203 were measured by real-time fluorescence quantitative PCR (RT-PCR).Results At the 8 th week of IgAN rat modeling, glomerular mesangial hyperplasia was observed. Comparing with normal controls, the expression of TLR4 and SOCS3 proteins and mRNA in kidney was significantly increased, and the miR-203 expression level was significantly elevated (P＜0.05). At the 9 th week of IgAN rat modeling, glomerular mesangial hyperplasia aggravated, the expression of TLR4 protein and mRNA did not change, but the expression of the SOCS3 protein and mRNA were significantly reduced the 8 th week (P＜0.05), but miR-203 expression was significantly increased (P＜0.05). Conclusion The expression of TLR4, SOCS3 and miR-203 in renal tissues of IgAN rat model is increased, which may be related to IgAN pathogenesis, and the SOCS3 expression decreases with the increase of mesangial hyperplasia, suggesting that SOCS3 may play a protective role in IgAN.