Vascular Endothelial Growth Factor-C Inhibits The Apoptosis Of Rat Renal Tubular Epithelial Cell

ObjectiveTo investigate the role of tumor necrosis factor-α(TNF-α)in the production ofvascular endothelial growth factor-C(VEGF-C) and its effect on cell apoptosis, andthen to discuss the impact of VEGF-C on renal tubular epithelial cell apoptosisinduced by TNF-α/actinomycin D (ActD).MethodsIn vivo, rats were divided into shamoperation group and UUO group. Theexpression and location of VEGF-C was measured by Western blot andimmunohistochemistry. Rat proximal renal tubular cell lines (NRK52E) were culturedin vitro. The control group was cultured by routine methods, and the experimentalgroup was cultured by TNF-αwith different concentration and different time. Realtime PCR and Western blotting were used to examine the mRNA and proteinexpression of VEGF-C. After treated with TNF-α/ActD for24h, cell apoptosis wasdetected by flow cytometry assay. Different concentration of VEGF-C was added toevaluate its protective role in cell apoptosis.ResultsVEGF-C expressed both in shamoperation group and UUO group, and locatedprimarily in the renal tubular wall. Compared with the shamoperation group, the level of VEGF-C was increased in UUO group. VEGF-C can be detected on nomalNRK52E cell. When treated with TNF-α, the mRNA and protein expression ofVEGF-C was increased in dose-and time-depandent manner. TNF-αcombined withActD could promote apoptosis in dose-depandent manner. The apoptosis could beinhibited by VEGF-C at50ng/ml, and at100ng/ml the inhibition goes to the highestdegree.ConclusionTNF-αup-regulates VEGF-C mRNA and protein expression. VEGF-C inhibitedapoptosis induced by TNF-α/ActD in dose-depandent manner.