通过调节NAMPT介导的NAD生物合成,TRAF3IP2驱动介酶干细胞衰老
Xiaoran Huang1, Baojuan Liu1, Yaowen Liang1,2
1Department of Emergency Medicine, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Heliyon
|October 9, 2023
概括
与TNF受体相关的3因子相互作用蛋白2 (TRAF3IP2) 通过AMPK通路降低NAMPT和NAD+水平,加速中细胞干细胞 (MSC) 衰老. 这为再生医学中衰老的MSCs的复苏提供了新的策略.
科学领域:
- 细胞生物学 细胞生物学
- 干细胞研究 干细胞研究
- 再生医学是一种再生医学.
背景情况:
- 中干细胞 (MSC) 中的细胞衰老阻碍了它们在再生医学中的应用.
- 与TNF受体相关的3因子相互作用蛋白2 (TRAF3IP2) 是一种促炎蛋白,在MSC衰老中没有明确的作用.
研究的目的:
- 研究TRAF3IP2在调节MSC衰老中的作用.
- 为了阐明TRAF3IP2诱导的MSC衰老的潜在机制.
主要方法:
- 使用与衰老相关的β-galactosidase (SA-β-gal) 染色来评估衰老.
- 量化了TRAF3IP2表达,衰老标志物,尼古丁胺氨酸二核酸 (NAD+) 水平和NAMPT表达.
- 采用了西式涂抹和NAD+水平测量.
主要成果:
- 与年轻的MSC (YMSC) 相比,老年MSC (AMSC) 的TRAF3IP2表达率较高.
- 过度表达TRAF3IP2加速了YMSC衰老;它的降低调节挽救了衰老.
- AMSCs显示NAMPT蛋白和NAD+水平降低,与抑制的AMPK信号传递有关.
- 通过AMPK抑制,TRAF3IP2通过降低NAMPT和NAD+的调节诱导衰老.
结论:
- TRAF3IP2通过AMPK通路抑制NAMPT介导的NAD+生物合成,从而加速MSC衰老.
- 针对TRAF3IP2或激活AMPK/NAMPT提供了一种新的方法来复兴老化的MSC.
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