Renal epithelial miR-205 expression correlates with disease severity in a mouse model of congenital obstructive nephropathy

Abstract

Background Congenital obstructive nephropathy (CON) is a leading cause of pediatric chronic kidney disease (CKD). Despite optimal surgical and medical care, there is a high rate of CKD progression. Better understanding of molecular and cellular changes is needed to facilitate development of improved biomarkers and novel therapeutic approaches in CON. Methods The megabladder (mgb) mouse is an animal model of CKD with impaired bladder emptying, hydronephrosis, and progressive renal injury. In this study, we characterize a particular microRNA, miR-205, whose expression changes with the degree of hydronephrosis in the mgb-/- kidney. Results Expression of miR-205 is progressively increased in the adult mgb-/-mouse with worsening severity of hydronephrosis. miR-205 expression is correlated with altered expression of cytokeratins and uroplakins, which are markers of cellular differentiation in urothelium. We describe the spatial pattern of miR-205 expression, including increased expression in renal urothelium and novel miR-205 expression in medullary collecting duct epithelium in the congenitally obstructed kidney. Conclusion miR-205 is increased with severity of congenital obstructive nephropathy and CKD in the mgb-/- mouse, and may regulate urothelial differentiation.

Long non-coding RNA GAS5 aggravate renal epithelial cell apoptosis in cisplatin-induced AKI by regulating miR-205-5p

“…The present study have some limitations: Initially, it was proved that CMTM4, ZEB2 and PTEN can perform as downstream regulators of miR-205-5p, and thus have the potential to be of importance in the GAS5's apoptosis modulation mechanism of cisplatin-induced AKI (10,21,26,(30)(31)(32)(33). Suggesting that they can be exerted as complementary indicators in follow-up studies to render the mechanism revealed more comprehensive.…”