Figure 6

Hepatocyte growth factor (HGF) or transforming growth factor (TGF)-β1 gene expression in kidney tissues. At the incipient stage (1 day), IRI triggered the upregulation of HGF/TGF-β1 expression, further promoted by nephrectomy or WJ-MSCs. At 1 week, WJ-MSCs remarkably induced the upregulation of HGF expression in damaged kidney tissue, thereby preventing the expression of HGF/TGF-β1 from decline to baseline. At 4 or 6 weeks, the HGF/TGF-β1 expression was substantially downregulated in vehicle-injected IRI rats, whereas this change was robustly prevented by cell injection or nephrectomy. The Ct (threshold cycle) for the target gene and β-actin was determined for each sample. The quantification of the target gene was normalized by β-actin. HGF/TGF-β1 was generated by referencing HGF expression to TGF-β1 expression. Gene expression in sham-treated samples was regarded as the calibrator (dotted line).The relative expression of HGF, TGF-β1, or HGF/TGF-β1 was calculated by 2^-ΔΔCt. Data are expressed as the mean of 2^-ΔΔCt ± SD of three rats for each experimental condition. xP < 0.05, IRI+WJ-MSCs versus IRI+VEHICLE; #P < 0.05, IRI+NEPHRECTOMY versus IRI+VEHICLE; ∗P < 0.01, IRI+VEHICLE versus SHAM. (a) through (d) graphs representing relative expression of HGF/β-actin, TGF-β1/β-actin, and HGF/TGF-β1 at 1 day, 1, 4, and 6 weeks after treatment, respectively.