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Pediatr Res ; 80(4): 602-9, 2016 10.
Article in English | MEDLINE | ID: mdl-27384406

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 CON and CKD in the mgb(-/-) mouse and may regulate urothelial differentiation.


Subject(s)
Epithelium/metabolism , Gene Expression Regulation , Kidney Diseases/congenital , MicroRNAs/genetics , Animals , Biomarkers/blood , Biomarkers/metabolism , Cell Differentiation , Disease Models, Animal , Disease Progression , Female , Hydronephrosis/blood , Keratins/blood , Kidney/metabolism , Kidney/pathology , Kidney Diseases/genetics , Kidney Diseases/physiopathology , Kidney Failure, Chronic/blood , Kidney Tubules, Collecting/metabolism , Male , Mice , Mice, Transgenic , Tight Junctions , Uroplakins/blood , Urothelium/metabolism , Urothelium/pathology
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