Xu Zhuojia, Diao Zongli, Liu Ruixia, Liu Wenhu
Department of Nephrology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, P.R. China.
Department of Infectious Disease, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, P.R. China.
Mol Med Rep. 2017 May;15(5):2560-2566. doi: 10.3892/mmr.2017.6307. Epub 2017 Mar 9.
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.
本研究的目的是探讨糖尿病肾病（DN）中Ski相关新蛋白N（SnoN）表达下调的调控机制。培养大鼠原代肾小管上皮细胞系NRK-52E细胞，以阐明在体外低葡萄糖环境中小母蛋白抑制因子2（Smurf2）对SnoN的影响。分别向NRK-52E细胞和糖尿病大鼠注射腺病毒AD-Smurf2和AD-shSmurf2，然后检测SnoN、Smurf2和磷酸化（p）-Smad2的蛋白表达谱。此外，用转化生长因子（TGF）-β1或TGF-β1抑制剂处理后，分析Smurf2、p-Smad2和SnoN的蛋白水平，以验证TGF-β1/Smad信号通路的作用。发现Smurf2通过泛素化作用对SnoN降解的影响是DN中的关键因素，这一过程由TGF-β1/Smad信号通路介导。
