S100A16-induced adipogenesis is associated with up-regulation of 11 beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1)
S100A16-induced adipogenesis is associated with up-regulation of 11 beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1)
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S100A16 诱导的脂肪生成与 1 型 11 β-羟基类固醇脱氢酶 (11 β-HSD1) 的上调有关
DOI：
10.1042/bsr20182042
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发表时间：
2019
影响因子：
4
通讯作者：
Liu Yun
中科院分区：
文献类型：
--
作者：
Zhang Rihua;Kan Jing Bao;Lu Shan;Tong Pei;Yang Jie;Xi Ling;Liang Xiubing;Su Dongming;Li Dong;Liu Yun
肥胖症的流行率持续以惊人的速度稳步上升，是一个重要的公共卫生问题，而S100 A16和11 β-羟基类固醇脱氢酶1型（11β-HSD 1）的表达变化可归因于脂肪细胞分化。在我们前期的研究中，我们发现在S100 A16过表达的3 T3-L1细胞模型中，11β-HSD 1蛋白表达增加。为了进一步研究S100 A16与11β-HSD 1的关系，以及S100 A16诱导脂肪形成的分子机制，我们构建了S100 A16转基因敲除小鼠和S100 A16过表达的3 T3-L1前脂肪细胞。采用S100 A16转基因（S100 A16 Tg/+）小鼠，分别饲喂正常脂肪饮食（NFD）和高脂饮食（HFD）模型，评价S100 A16对脂肪形成、11β-HSD 1表达以及基因表达的RNA测序和定量的影响。使用3 T3-L1细胞模型，我们检测了S100 A16和11β-HSD 1对前脂肪细胞分化的影响，以及S100 A16诱导的11β-HSD 1过表达的细胞信号事件。我们发现，与C57 BL/6小鼠相比，HFD条件下S100 A16的过表达增加了WAT的脂质含量和肝细胞的脂肪浸润，11β-HSD 1蛋白的表达沿着S100 A16的增加。S100 A16和11β-HSD 1的高表达促进3 T3-L1细胞的脂肪形成。过表达S100 A16可抑制11β-HSD 1的降解。我们的结论是，S100 A16诱导的脂肪形成与11β-HSD 1的上调有关。
The steadily increasing epidemic of obesity continues at alarming rates, is an important public health problem, and expression changes of S100A16 and 11 β-hydroxysteroid dehydrogenase type 1(11β-HSD1) is attributable to the adipocyte differentiation. In our previous study, we found that 11β-HSD1 protein expression increased in S100A16-overexpressed 3T3-L1 cell model. In order to further investigate the relationship between S100A16 and 11β-HSD1, and the molecular mechanisms of S100A16-induced adipogenesis, we constructed S100A16 transgenic and knockout mouse, and S100A16-overexpressed 3T3-L1 preadipocyte cell. Using S100A16 transgenic (S100A16Tg/+) mice fed with normal fat diet (NFD) and high fat diet (HFD) diet model, we evaluated the effect of S100A16 on adipogenesis, expression of 11β-HSD1, and RNA sequencing and quantification of gene expression. Using the 3T3-L1 cell model, we examined the effect of S100A16 and 11β-HSD1 on pre-adipocyte differentiation, and cell signaling events of 11β-HSD1 overexpression induced by S100A16. We found that when compared with C57BL/6 mice, overexpression of S100A16 under the condition of HFD increased lipid content in WAT and fat infiltration in hepatocytes, 11β-HSD1 protein expression increased along with S100A16. Elevated S100A16 and 11β-HSD1 expression promoted adipogenesis in 3T3-L1 cells. Overexpression of S100A16 inhibited the degradation of 11β-HSD1. We conclude that S100A16-induced adipogenesis is associated with up-regulation of 11β-HSD1.