Department of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei 050017, P.R. China.
Department of Pathology, The Third Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, P.R. China.
Mol Med Rep. 2023 Feb;27(2). doi: 10.3892/mmr.2023.12929. Epub 2023 Jan 5.
Tubulointerstitial fibrosis (TIF) is an important pathological change that occurs during the development of diabetic kidney disease. The epithelial‑mesenchymal transition (EMT) of renal tubular epithelial cells is a manifestation of TIF. STAT1, a member of the STAT family of transcription factors, can be modified by the small ubiquitin‑related modifier (SUMO), thus affecting the activity of STAT1. The present study investigated the role of STAT1 SUMOylation in high glucose‑induced tubular EMT by western blotting, immunocytochemistry, immunofluorescence, co‑immunoprecipitation and dual luciferase reporter analysis. The results indicated that in the process of high glucose‑induced EMT, STAT1 activation protected the cells from EMT. However, high glucose also increased the SUMOylation of STAT1, which prevented STAT1 from exerting an effective protective role by inhibiting its activity.
肾小管间质纤维化(TIF)是糖尿病肾病发展过程中发生的重要病理变化。肾小管上皮细胞的上皮-间充质转化(EMT)是 TIF 的表现形式。STAT1 是 STAT 转录因子家族的成员,可被小泛素相关修饰物(SUMO)修饰,从而影响 STAT1 的活性。本研究通过 Western blot 印迹、免疫细胞化学、免疫荧光、共免疫沉淀和双荧光素酶报告基因分析,探讨了 STAT1 SUMO 化在高糖诱导的管状 EMT 中的作用。结果表明,在高糖诱导的 EMT 过程中,STAT1 的激活保护细胞免受 EMT 的影响。然而,高糖还增加了 STAT1 的 SUMO 化,通过抑制其活性,阻止 STAT1 发挥有效的保护作用。