FTO通过破坏NOLC1mRNA的稳定性来抑制牙真菌干细胞衰老
Bingrong Li1, Mi Xu1, Junjun Huang1
1State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan 430072, China.
Biomolecules
|November 27, 2025
概括
脂肪质量和与肥胖相关的蛋白质 (FTO) 调节牙髓干细胞 (DPSC) 的衰老. 由于FTO的耗尽,通过提高NOLC1的调节,加速DPSC衰老,为再生医学提供了洞察力.
科学领域:
- 干细胞生物学 干细胞生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 老龄化的分子机制.
背景情况:
- 细胞衰老会损害干细胞的功能.
- 脂肪质量和与肥胖相关的 (FTO) 蛋白质影响干细胞的命运.
- FTO在牙髓干细胞 (DPSC) 衰老中的作用尚不清楚.
研究的目的:
- 调查FTO在DPSC衰老中的作用.
- 阐明FTO在DPSC衰老中的功能背后的分子机制.
主要方法:
- 在老化的DPSC中评估FTO表达.
- 操纵的FTO水平 (耗尽/过度表达) 和评估的DPSC增殖,衰老标志物和活性氧物种 (ROS).
- 利用RNA测序来识别FTO目标,并研究FTO/NOLC1/p53信号通路.
主要成果:
- 在DPSC衰老期间,FTO表达减少.
- FTO耗尽加速衰老和增加ROS;FTO过度表达具有相反的效果.
- FTO敲击抑制了rRNA前生物发生,上调NOLC1,通过核应激和p53积累促进衰老. NOLC1的淘汰部分挽救了FTO缺陷引起的衰老.
结论:
- 发现了一种新的FTO/NOLC1/p53轴调节DPSC衰老.
- FTO下调稳定了NOLC1mRNA,抑制了rRNA前转录并诱导衰老.
- 结果为预防DPSC衰老提供了洞察力,用于再生医学应用.
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