索克斯6通过向酸氧化酶和前脂细胞因子1来损害介质干细胞的脂肪生成承诺
Shao-Yue Du1, Liang Hu1, Bing-He Zhou1
1Department of Clinical Laboratory, Shanghai Pudong Hospital, Obstetrics and Gynecology Hospital, Fudan University, Shanghai, 201399, China.
Biochemical and biophysical research communications
|October 2, 2023
概括
一个关键的调节剂Sox6,抑制了介酶干细胞 (MSC) 分化成脂肪细胞的过程. 向Sox6可能通过控制脂肪细胞发育,为肥胖和代谢障碍提供新的治疗方法.
科学领域:
- 细胞生物学 细胞生物学
- 代谢科学 代谢科学
- 分子生物学分子生物学
背景情况:
- 介酶干细胞 (MSC) 分化成脂肪细胞对于能量平衡至关重要.
- 控制MSC承诺和脂肪细胞分化终止的机制尚未完全理解.
- 转录因子Sox6 (性别决定区域Y (SRY) -box6) 在脂肪生成调节中的作用在很大程度上尚未被探索.
研究的目的:
- 研究Sox6在调节脂肪细胞分化中的作用.
- 探索Sox6在前脂肪细胞发育和脂生成分化的终止中的功能.
主要方法:
- 在C3H10T1/2细胞 (体外) 和C57BL/6J小鼠 (体内) 中过度表达Sox6.
- 从肥胖和对照小鼠的脂肪组织中分析Sox6表达.
- 对Sox6与lysyl氧化酶 (Lox) 和前脂质细胞因子1 (Pref1) 促进体结合的研究,含有或不含 histone deacetylase-1 (HDAC1).
主要成果:
- 与对照小鼠相比,肥胖小鼠的脂肪组织中观察到Lower Sox6表达.
- Sox6的过度表达抑制了MSC的分化到脂肪细胞.
- Sox6直接与Lox和Pref1促进体结合,这种相互作用由HDAC1.1增强.
结论:
- 索克斯6是MSC对脂肪细胞血统的承诺的关键调节者.
- 在肥胖和相关的代谢障碍方面,Sox6介导调节是一个潜在的治疗标.
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