Published in:
01-12-2018 | Original article
Expression of β-catenin in regenerating renal tubules of cisplatin-induced kidney failure in rats
Published in: Clinical and Experimental Nephrology | Issue 6/2018
Login to get accessAbstract
Background
β-Catenin is a multi-functional protein involved in nephrogenesis and also plays important roles in renal injury. Here, the expression of β-catenin was investigated in the proximal renal tubular epithelial cells in cisplatin (CDDP)-induced acute kidney injury (AKI) and chronic kidney injury (CKI), because CDDP-induced renal lesions were characterized by proximal renal tubular epithelial degeneration/regeneration and subsequent interstitial fibrosis.
Methods
F344 rats were treated with CDDP. The expression of β-catenin and proliferative (Ki67) or fibrogenic [vimentin, α-smooth action (α-SMA)] markers was analyzed by immunolabeling.
Results
β-Catenin, vimentin and Ki67 were not seen in the proximal renal tubules of control rats. Interestingly, in CDDP-induced AKI, the regenerating proximal renal tubular epithelial cells reacting strongly with Ki67 expressed membranous or cytoplasmic β-catenin and also showed a positive reaction to vimentin but not to α-SMA. In CDDP-induced CKI, the epithelial cells of abnormally dilated or atrophied renal tubules did not react to β-catenin or Ki67, but showed positive reactions to vimentin and α-SMA. β-Catenin mRNAs were significantly increased in AKI and significantly decreased in CKI.
Conclusion
Newly expressed β-catenin in the proximal renal tubules after AKI may participate in functional regeneration. In CKI, epithelial cells of abnormal renal tubules did not express β-catenin but reacted to vimentin, and α-SMA might indicate the epithelial–mesenchymal transition (EMT) formation, because α-SMA is usually expressed in myofibroblasts forming via EMT. The presence or absence of β-catenin expression would become a marker for the EMT phenomenon in progressive renal fibrosis.