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首页> 外文期刊>Pediatric Research >Effects of SOCS 1/3 gene silencing on the expression of C/EBPα and PPARγ during differentiation and maturation of rat preadipocytes
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Effects of SOCS 1/3 gene silencing on the expression of C/EBPα and PPARγ during differentiation and maturation of rat preadipocytes

机译:SOCS 1/3基因沉默对大鼠前脂肪细胞分化和成熟过程中C /EBPα和PPARγ表达的影响

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Background:Suppressor of cytokine signaling-1 and -3 (SOCS-1 and SOCS-3) are two important negative regulators in the insulin-signaling pathway, and their overexpression may aggravate insulin resistance. Subjects with insulin resistance are often obese and have increased expressions of SOCS-1 and SOCS-3. We speculated that SOCS-1 and SOCS-3 may be involved in abnormal deposition of adipose tissues during insulin resistance.Methods:A catch-up growth intrauterine growth retardation (CG-IUGR) rat model with insulin resistance was established; mRNA and protein expression of SOCS-1, SOCS-3, the CCAAT/enhancer binding protein (C/EBPα), and peroxisome proliferator-activated receptor (PPARγ) in adipose tissue were measured by real-time PCR and western blot; plasmids carrying small hairpin RNAs (shRNAs) targeting the SOCS-1 and SOCS-3 genes were constructed and transfected into preadipocytes, which were then induced to mature. At 72?h after differentiation was induced, the expressions of C/EBPα and PPARγ, two important molecules promoting the differentiation of preadipocytes, were detected.Results:Expressions of SOCS-1, SOCS-3, C/EBPα, and PPARγ were markedly increased in adipose tissues of CG-IUGR rats, whereas the expressions of C/EBPα and PPARγ were significantly reduced after gene silencing of SOCS-1 or SOCS-3 in adipocytes.Conclusion:Overexpression of SOCS-1 and SOCS-3 may enhance the expression of C/EBPα and PPARγ, resulting in abnormal deposition of adipose tissues during insulin resistance.
机译:背景:细胞因子信号传导-1和-3的抑制因子(SOCS-1和SOCS-3)是胰岛素信号传导通路中的两个重要的负调控因子,它们的过度表达可能加剧胰岛素抵抗。具有胰岛素抵抗的受试者通常是肥胖的并且具有增加的SOCS-1和SOCS-3的表达。我们推测SOCS-1和SOCS-3可能参与了胰岛素抵抗过程中脂肪组织的异常沉积。方法:建立具有胰岛素抵抗的追赶生长宫内生长迟缓(CG-IUGR)大鼠模型;实时荧光定量PCR和蛋白质印迹法检测脂肪组织中SOCS-1,SOCS-3,CCAAT /增强子结合蛋白(C /EBPα)和过氧化物酶体增殖物激活受体(PPARγ)的mRNA和蛋白表达;构建携带针对SOCS-1和SOCS-3基因的小发夹RNA(shRNA)的质粒,并将其转染到前脂肪细胞中,然后诱导成熟。诱导分化后72h,检测到促进前脂肪细胞分化的两个重要分子C /EBPα和PPARγ的表达。结果:SOCS-1,SOCS-3,C /EBPα和PPARγ的表达明显SOCS-1或SOCS-3基因沉默后,脂肪细胞中CG-IUGR大鼠脂肪组织中C /EBPα和PPARγ的表达显着降低。结论:SOCS-1和SOCS-3的过表达可能增强了脂肪细胞中SOCS-1和SOCS-3的表达。 C /EBPα和PPARγ的表达异常,导致胰岛素抵抗期间脂肪组织异常沉积。

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