删除CD44通过调节PPARγ和细胞循环相关途径来促进脂肪生成
Xiong Weng1, Hao Jiang2, David J Walker1
1Division of Cellular and Systems Medicine, School of Medicine, University of Dundee, Dundee, Scotland, UK.
The Journal of endocrinology
|May 1, 2024
概括
细胞受体CD44调节脂肪细胞的发育和功能. 移除CD44可以改善脂肪细胞分化和胰岛素敏感性,为代谢疾病提供潜在的治疗点.
科学领域:
- 细胞生物学 细胞生物学
- 代谢性疾病研究研究
- 脂肪细胞生物学 脂肪细胞生物学
背景情况:
- 细胞表面受体和干细胞生物标志物CD44越来越多地与慢性代谢障碍有关.
- 与肥胖相关的脂肪组织炎症和胰岛素抵抗可以通过CD44切除来改善.
研究的目的:
- 研究人类和小鼠脂肪组织中不同细胞类型中的CD44表达.
- 确定CD44在前脂肪细胞中调节脂肪细胞功能和分化中的作用.
主要方法:
- 在3T3-L1细胞中,CRISPR-Cas9基因删除和lentivirus介导的基因再表达.
- 定量蛋白质组学分析以确定受影响的细胞通路.
- 评估脂肪细胞分化,胰岛素响应,脂蛋白分泌和前脂肪细胞增殖率.
主要成果:
- CD44删除增强了脂肪细胞分化和脂肪生成.
- CD44的再表达降低了胰岛素的反应和平蛋白的分泌,抑制了脂肪生成,并降低了前脂肪细胞的增殖.
- CD44似乎通过抑制PPARγ表达和影响细胞循环途径来调节脂肪生成.
结论:
- 前脂肪细胞中的CD44在调节脂肪生成和脂肪细胞功能方面发挥着重要作用,独立于其在免疫细胞中的已知作用.
- 在 (前) 脂肪细胞中向CD44为与肥胖相关的代谢并发症提供了潜在的治疗策略.
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