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首页> 外文期刊>Cell death and differentiation >G0/G1 switch gene 2 has a critical role in adipocyte differentiation
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G0/G1 switch gene 2 has a critical role in adipocyte differentiation

机译：G0 / G1开关基因2在脂肪细胞分化中起关键作用

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Mouse 3T3-L1 preadipocytes differentiate into adipocytes when treated with 3-isobutyl-1-methylxanthine, dexamethasone, and insulin. Although mechanisms of adipogenesis, including transcriptional cascades, are understood, it is still unclear how clonally expanded cells eventually enter the terminal differentiation program. From gene expression profile studies, we identified G0/G1 switch gene 2 (G0s2) as a novel regulator of adipogenesis. The gene was found to be expressed at a higher level in white and brown adipose tissues, and it was induced in 3T3-L1 cells by hormonal treatment. Importantly, G0s2 expression was closely associated with the transition from mitotic clonal expansion to terminal differentiation. Knockdown of G0s2 expression with siRNA inhibited adipocyte differentiation, whereas constitutive overexpression of G0s2 accelerated differentiation of preadipocytes to mature adipocytes. Expression of G0s2 was found to be regulated by peroxisome proliferator-activated receptor γ (PPARγ), which is a well-known regulator of adipocyte differentiation. Absence of either PPARγ or G0s2 expression resulted in apoptotic pathway activation before terminal differentiation. To determine whether G0s2 has a role in vivo, G0s2-knockout mice were generated. The knockout mice were normal in appearance, but they had less adipose mass than wild-type littermates. Mouse embryonic fibroblast cells from G0s2-deficient mice exhibited impaired adipogenesis and contained unusually small intracellular lipid droplets, suggesting that G0s2 has a role in lipid droplet formation. Our studies demonstrate that G0s2 has an important role in adipogenesis and accumulation of triacylglycerol.
机译：小鼠3T3-L1前脂肪细胞经3-异丁基-1-甲基黄嘌呤，地塞米松和胰岛素处理后可分化为脂肪细胞。尽管已经了解了脂肪生成的机制，包括转录级联反应，但仍不清楚克隆扩增的细胞如何最终进入末端分化程序。从基因表达谱研究，我们确定G0 / G1开关基因2（G0s2）作为脂肪形成的新型调节剂。发现该基因在白色和棕色脂肪组织中高水平表达，并通过激素处理在3T3-L1细胞中被诱导。重要的是，G0s2表达与从有丝分裂克隆扩增到终末分化的转变密切相关。用siRNA抑制G0s2表达可抑制脂肪细胞的分化，而G0s2的组成型过表达则加速了前脂肪细胞向成熟脂肪细胞的分化。发现G0s2的表达受过氧化物酶体增殖物激活受体γ（PPARγ）的调节，PPARγ是众所周知的脂肪细胞分化调节剂。 PPARγ或G0s2表达的缺失会导致终末分化之前凋亡途径的激活。为了确定G0s2是否在体内起作用，生成了G0s2基因敲除小鼠。剔除小鼠的外观正常，但脂肪量少于野生型同窝仔。来自G0s2缺陷型小鼠的小鼠胚胎成纤维细胞表现出脂肪形成受损，并含有异常小的细胞内脂质小滴，表明G0s2在脂质小滴形成中起作用。我们的研究表明，G0s2在三酰基甘油的脂肪生成和积累中具有重要作用。

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