The miRNA-184 drives renal fibrosis by targeting HIF1AN in vitro and in vivo

AbstractProgressive renal fibrosis is the last phase of chronic kidney disease and results in renal failure. Micro-RNA has been demonstrated as important agent to drive organ fibrosis. However, the precise mechanisms are not fully understood. Here, we found miRNA-184 as a critical mediator to promote the renal fibrosis by targeting HIF1AN. In Vivo, miRNA-184 expression levels remarkably increased both in patients ’ serum and in unilateral ureteral obstruction kidneys, as well as induced the expression of COL1A1 and COL3A1. Furthermore, transfection of NRK49F cells with miRNA-184 mimics down-regulated HIF1AN, transfection of NRK49F cells with miRNA-184 inhibitor up-regulated HIF1AN, while the cells transfec ted with miRNA-184 inhibitor exerted the opposite effect. When the cells were co-transfected with miRNA-184 mimics and HIF1AN, the expression of α-SMA, GTGF, COL1A1, and COL3A1 at mRNA level was apparently decreased when compared with miRNA-184 mimic-transfected cells, which was strengthened when t ransfected with miRNA-184 inhibitor. Thus, miRNA-184 is an important agent to promote the fibrosis though binding to HIF1AN, and may be a promising novel target in treatment of renal fibrosis.
Source: International Urology and Nephrology - Category: Urology & Nephrology Source Type: research