De novo expression of human leukocyte antigen-DR (HLA-DR) and loss of beta-catenin expression in tubular epithelial cells: A possible event in epithelial–mesenchymal transition in canine renal diseases

Tubulointerstitial fibrosis (TIF) plays a central role in the progression to end-stage renal disease. Tubular epithelial cells (TECs) undergo epithelial–mesenchymal transition (EMT) and may contribute to the progression of TIF. Using immunohistochemistry, the primary aim of this study was to assess the expression of β-catenin, human leukocyte antigen-DR (HLA-DR) and vimentin in renal biopsies from dogs with spontaneous kidney diseases of varying severities. Morphological diagnosis, severity of inflammation, TIF, HLA-DR expression and clinicopathological variables were compared in dogs with renal injury to identify any potential relationship between the different factors; β-catenin down-regulation was used as a marker of EMT. is, HLA-DR expression, serum creatinine concentration (SCr), and urine protein-to-creatinine ratio (UPC) were all increased and β-catenin expression decreased in dogs with primary glomerular disease compared with dogs with acute tubular necrosis. HLA-DR expression by TECs was positively correlated to fibrosis, inflammation, UPC, and SCr. β-catenin expression was negatively correlated to fibrosis, inflammation and HLA-DR expression. The progression of renal failure correlated closely with tubulointerstitial damage. De novo HLA-DR expression associated with β-catenin down-regulation by TECs may represent a possible step in the progression of TIF and EMT.