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多omics方法揭示了TGF-β信号驱动的衰老周期性干细胞中的衰老

Bo Li¹, Wei Li², Yueqi Liao³

¹State Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Department of Orthodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.

Journal of advanced research

|January 1, 2025

概括

转化生长因子-β1 (TGF-β1) 通过DNA甲基化和活性氧物种 (ROS) 生产诱导牙周带干细胞 (PDLSC) 衰老. 抑制ROS或逆转表观遗传沉默可以缓解这种衰老,为牙周疾病提供治疗潜力.

科学领域:

干细胞生物学干细胞生物学
牙周研究牙周研究
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:

牙周带干细胞 (PDLSCs) 维护牙的完整性.
PDLSC功能障碍和衰老有助于与年龄相关的牙周疾病和牙脱落.
转化生长因子-β1 (TGF-β1) 在PDLSC衰老中的作用尚不清楚.

研究的目的:

阐明TGF-β1在PDLSC衰老中的作用.
为了确定驱动TGF-β1诱导的PDLSC衰老的分子机制.
为发展与年龄相关的牙周疾病的向治疗提供信息.

主要方法:

空间转录组学用于绘制Tgfb1 mRNA表达在小鼠骨组织中的地图.
伪时代分析以推断时间表达力学.
使用人类PDLSCs进行体外研究,以评估TGF-β1对DNA甲基化,衰老,细胞循环和信号通路的影响.

主要成果:

丰富的Tgfb1表达被观察到在周期.
TGF-β1治疗诱导了PDLSC衰老,G2细胞循环停止和活性氧物种 (ROS) 的增加.
TGF-β1诱导的ROS产生是由于DNA甲基化介导的PRKAG2沉默 (编码AMPKγ2),激活ATM信号. 抑制ROS或PRKAG2表观遗传逆转缓解老化.

结论:

这项研究提供了第一个在空间上解析的转录基因图像,用于小鼠骨组织.
鉴定出DNA甲基化是TGF-β1诱导的PDLSC衰老的一个关键机制.
研究结果揭示了TGF-β1,ROS和表观遗传调节之间的联系,这表明牙周病的新疗法策略.

关键词:

细胞衰老细胞衰老通过DNA甲基化.牙周带干细胞 (PDLSCs) 是一种干细胞.反应性氧物种 (ROS) 是一种反应性氧物种.空间转录组学空间转录组学转化生长因子-β (TGF-β) 的转化生长因子-β

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