ILK participates in renal interstitial fibrosis by altering the phenotype of renal tubular epithelial cells via TGF-β1/smad pathway

OBJECTIVE: To explore the specific role of ILK (integrin-linked kinase) in regulating renal fibrosis and its underlying mechanism. MATERIALS AND METHODS: NRK-52E cells were induced by transforming growth factor-beta 1 (TGF-beta 1) for observing phenotype change. Renal tubular epithelial cell marker, fibrosis marker and expression level of ILK in NRK-52E cells were also detected. After overexpression of ILK, phenotype change of NRK-52E cells was observed. For in vivo experiments, we constructed UUO (unilateral ureteral obstruction) model in CD1 mice. Renal tubular epithelial cell marker, fibrosis marker and expression level of ILK in UUO mice were detected. The regulatory effect of ILK on renal fibrosis was detected after injection of ILK over expression plasmid. Western blot was performed to detect related genes in the TGF-beta 1/smad pathway. RESULTS: Accompanied by the TGF-beta 1-induced phenotype change in NRK-52E cells, both mRNA and protein levels of ILK were upregulated. Overexpression of ILK remarkably stimulated the phenotype change in NRK-52E cells. Similarly, ILK was highly expressed in UUO mice. Renal fibrosis was aggravated after injection of ILK overexpression plasmid in UUO mice. Western blot results showed that expressions of p-smad3 and smad3 were upregulated during the process of renal fibrosis. CONCLUSIONS: ILK is upregulated during the process of renal fibrosis. ILK participates in the development of renal fibrosis by altering phenotypes of renal tubular epithelial cells via a TGF-beta 1/smad pathway.