The aim of the present study was to examine the regulatory mechanism underlying the depression in Ski-related novel protein N (SnoN) in diabetic nephrology (DN). NRK-52E cells, a rat primary renal tubular epithelial cell line, were cultured to clarify the effect of small mothers against decapentaplegic (Smad) ubiquitination regulatory factor 2 (smurf2) on SnoN in a low glucose environment in vitro. NRK-52E cells and DM rats were injected with adenoviruses AD-smurf2 and AD-shsmurf2, respectively, and the protein expression profiles of SnoN, smurf2 and phosphorylated (p)-Smad2 were then detected. In addition, the protein levels of smurf2, p-Smad2 and SnoN were analyzed following treatment with transforming growth factor (TGF)-β1 or TGF-β1 inhibitor to validate the effect of the TGF-β1/Smad signaling pathway. The effect of smurf2 on the degradation of SnoN by ubiquitination was found to be a key factor in DN, which was mediated by the TGF-β1/Smad signaling pathway.
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