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目的探讨肿瘤坏死因子-α(TNF-α)对人脂肪细胞STEAP4蛋白膜转位的影响,并分析其可能的机制。方法应用1-甲基-3-异丁基黄嘌呤(MIX)、地塞米松、胰岛素、罗格列酮方案诱导人前体脂肪细胞分化,以人重组TNF-α或加用细胞外信号调节蛋白激酶(ERK)抑制剂PD-98059干预人成熟脂肪细胞24 h,采用Western blot技术检测细胞膜蛋白与总蛋白中STEAP4蛋白的表达。结果 TNF-α干预能显著促进人成熟脂肪细胞中STEAP4蛋白向细胞膜转位;ERK抑制剂PD-98059联合TNF-α与单独应用TNF-α诱导人成熟脂肪细胞的细胞膜蛋白和总蛋白中STEAP4蛋白的表达水平比较均无显著差异。结论 TNF-α干预显著促进人成熟脂肪细胞中STEAP4蛋白的膜转位,初步排除丝裂原活化蛋白激酶信号途径参与这一调控机制。
Objective To investigate the effect of tumor necrosis factor-α (TNF-α) on the translocation of STEAP4 protein in human adipocytes and to analyze its possible mechanism. Methods Human adipocyte differentiation was induced by using 1-methyl-3-isobutylxanthine (MIX), dexamethasone, insulin and rosiglitazone regimen. Human recombinant TNF-α or extracellular signal-regulated PD-98059, an inhibitor of protein kinase (ERK), was used to treat human mature adipocytes for 24 h. Western blot was used to detect the expression of STEAP4 protein in the plasma membrane protein and total protein. Results TNF-αinduced STEAP4 protein translocation in human mature adipocytes. ERK inhibitor PD-98059 combined with TNF-α and TNF-α alone induced the expression of STEAP4 in cell membrane protein and total protein of human mature adipocytes There was no significant difference in the expression levels between the two groups. Conclusion The intervention of TNF-α can significantly promote the membrane translocation of STEAP4 in human mature adipocytes, and initially exclude the mitogen-activated protein kinase signaling pathway in this regulatory mechanism.