Abstract
E-cadherin expression in the kidney is used as a surrogate marker of epithelial mesenchymal transition for the testing of various antifibrotic strategies. Here we reexamined E-cadherin expression in the kidneys of rats with unilateral ureteric obstruction, which was previously reported to decrease in parallel with the development of tubulointerstitial disease in this widely used experimental model of renal fibrosis and epithelial mesenchymal transition. E-cadherin mRNA expression was consistently increased both acutely (hours) and chronically (days) in the ligated kidney compared to the cognate non-ligated kidney. Increased E-cadherin protein levels were also found in the ligated kidney particularly in dilated tubular segments. Simulation of early pressure changes in the ligated kidney by mechanical stretch of human renal epithelial cells in culture did not alter E-cadherin expression. Porcine LLCPK-1 cells subjected to hypotonic stretch, however, did have increased E-cadherin mRNA and protein levels, responses that were not prevented by transforming growth factor-beta, a cytokine that promotes epithelial mesenchymal transition. Our findings question the utility of E-cadherin as a marker of epithelial mesenchymal transition in this model of renal fibrosis.