S-G Zhou1, H-J Ma, Z-Y Guo, W Zhang, X Yang. 1. Department of Nephrology, Jining No. 1 People's Hospital, Jining, China. snkzhou@126.com.
Abstract
OBJECTIVE: To investigate the potential role of FHL2 (four and a half LIM domains protein 2) in the renal interstitial fibrosis and its underlying mechanism. MATERIALS AND METHODS: NRK-52E, the rat tubular epithelial cell line, was selected for the in vitro experiments. The unilateral ureteral obstruction (UUO) mouse model and phenotype changes of NRK-52E cells were induced by TGF-β (transforming growth factor-β) treatment. Protein and mRNA expressions of biomarkers of tubular cells and renal fibrosis in NRK-52E cells were detected. Meanwhile, phenotype changes of NRK-52E cells were detected after FHL2 overexpression. Furthermore, CD1 mice were selected for constructing the UUO mouse model. Protein and mRNA expressions of biomarkers of tubular cells and renal fibrosis in kidney tissues were detected. CD1 mice with FHL2 overexpression were constructed by tail vein injection of FHL2 plasmid for further observation of renal interstitial fibrosis. Expressions of β-catenin pathway-related genes were detected by Western blot and polymerase chain reaction (PCR), respectively. RESULTS: The FHL2 expression was increased during the phenotype change of NRK-52E cells induced by TGF-β treatment. Overexpression of FHL2 led to a significant phenotype change. Similarly, the FHL2 expression was elevated in the UUO mouse model. Renal interstitial fibrosis was exaggerated and expression levels of genes related to the β-catenin pathway were increased after injection of FHL2 plasmid. CONCLUSIONS: FHL2 is involved in renal interstitial fibrosis by altering the phenotype of renal tubular epithelial cells via regulating the β-catenin pathway.
OBJECTIVE: To investigate the potential role of FHL2 (four and a half LIM domains protein 2) in the renal interstitial fibrosis and its underlying mechanism. MATERIALS AND METHODS: NRK-52E, the rat tubular epithelial cell line, was selected for the in vitro experiments. The unilateral ureteral obstruction (UUO) mouse model and phenotype changes of NRK-52E cells were induced by TGF-β (transforming growth factor-β) treatment. Protein and mRNA expressions of biomarkers of tubular cells and renal fibrosis in NRK-52E cells were detected. Meanwhile, phenotype changes of NRK-52E cells were detected after FHL2 overexpression. Furthermore, CD1mice were selected for constructing the UUO mouse model. Protein and mRNA expressions of biomarkers of tubular cells and renal fibrosis in kidney tissues were detected. CD1mice with FHL2 overexpression were constructed by tail vein injection of FHL2 plasmid for further observation of renal interstitial fibrosis. Expressions of β-catenin pathway-related genes were detected by Western blot and polymerase chain reaction (PCR), respectively. RESULTS: The FHL2 expression was increased during the phenotype change of NRK-52E cells induced by TGF-β treatment. Overexpression of FHL2 led to a significant phenotype change. Similarly, the FHL2 expression was elevated in the UUO mouse model. Renal interstitial fibrosis was exaggerated and expression levels of genes related to the β-catenin pathway were increased after injection of FHL2 plasmid. CONCLUSIONS:FHL2 is involved in renal interstitial fibrosis by altering the phenotype of renal tubular epithelial cells via regulating the β-catenin pathway.