Experimental Study Of High Glucose Induced Renal Epithelial-Messenchymal-Transition Through TGF-β1/Smad Pathway

Objective: To investigate the effect of high glucose on renal tubular Epithelial-Mesenchymal transition and evaluate the relationship between high glucose and transforming growth factorβ1.Methods: HKC and Smad7-overexpression HKC cells were grown in DMEM/F12 medium containing 5%-10% newborn calf serum. They were cultured for 16h in free serum medium as well as 80% cells were adhered onto the surface of the flask. Afterwards, they were stimulated by high glucose (glucose concentration: 25mmol/1 and 50mmol/1). Western Blot detected the expression ofα-SMA, E-cadherin and ELISA detected Fibronectin while the expression of TGF-β1.Results: In HKC induced by high glucose,α-SMA and Fibronectin proteins were highly expressed while E-cadherin protein was down regulated. Besides, a dose-dependent up-regulated of TGF-β1 was also detected. These above-mentioned effects can be obviously inhibited by anti-TGF-β1 antibody. The expression ofα-SMA, Fibronectin and E-cadherin proteins were no change in Smad7-overexpression HKC induced by high glucose.Conclusion: High glucose may induce renal tubular Epithelial-Messenchymal transition through TGF-β1 pathway, which can be inhibited blocking the Smad signal pathway.