Search for Molecular Markers of Myocardial Injury in a Mouse Model of Obstructive Nephropathy Using Nestin Promoter-Driven GFP Expression.

Abstract

The expression of cardiac dysfunction markers and the number of nestin-positive cells in the myocardium were analyzed in a mouse model of obstructive nephropathy using animals expressing GFP under the nestin promoter. Unilateral ureteral obstruction (UUO) led to an increase in the number of nestin-positive cells in cardiac tissue, accompanied by elevated expression of B-type natriuretic peptide, which positively correlated with GFP levels. A trend toward reduced expression of β-myosin heavy chain and the gap junction protein connexin-43 was observed, whereas the expression of the progenitor cell marker WT1 remained unchanged under UUO conditions. These findings indicate the development of cardiac dysfunction in this model is secondary to primary renal injury and highlight a concomitant expansion of nestin-positive cells within the myocardium.