Abstract
MicroRNA (miR)-98-5p has been reported to be involved in the development of lupus nephritis (LN); however, its specific role in LN remains unclear. The present study aimed to investigate the effect of miR-98-5p on human mesangial cell proliferation and the secretion of TNF-α and IL-6. Reverse transcription-quantitative PCR (RT-qPCR) and western blotting were used to analyze the level of gene and protein expression, respectively. Cellular proliferation was assessed using a Cell Counting Kit-8 (CCK-8) assay. ELISA was used to detect the secretion of TNF-α and IL-6 by human mesangial cells. RT-qPCR analysis revealed that miR-98-5p expression was downregulated in LN renal tissues compared with control renal tissues. Overexpression of miR-98-5p inhibited human mesangial cell proliferation and the secretion of TNF-α and IL-6, whereas miR-98-5p-knockdown demonstrated the opposite effect. Dual luciferase reporter assays demonstrated that miR-98-5p directly targeted BTB and CNC homology 1 (BACH1). BACH1-overexpression promoted human mesangial cell proliferation and the secretion of TNF-α and IL-6, whereas BACH1-knockdown demonstrated the opposite effect. Notably, co-transfection with miR-98-5p mimic inhibited BACH1-overexpression induced human mesangial cell proliferation and the secretion of TNF-α and IL-6. The results of the present study indicated that miR-98-5p inhibited human mesangial cell proliferation and the secretion of TNF-α and IL-6 by targeting BACH1. Therefore, miR-98-5p and BACH1 may represent potential therapeutic targets for LN.
Keywords:
BTB and CNC homology 1; human mesangial cell; lupus nephritis; microRNA-98-5p; proliferation.