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与年龄相关的ECM刚度介导肌肉干细胞分化中的TRAIL激活

Amira A Alakhdar¹, Sruthi Sivakumar², Rylee M Kopchak³

¹Department of Chemistry, Carnegie Mellon University, Pittsburgh, PA, 15213, USA.

Advanced biology

|November 27, 2024

概括

衰老会使肌肉细胞外基质变硬,损害干细胞的再生. 这项研究揭示了TNF相关的诱导亡联体 (TRAIL) 途径在硬基质上老化的细胞中激活,导致肌肉功能障碍.

科学领域:

肌肉干细胞生物学肌肉干细胞生物学
细胞外基质衰老细胞外基质衰老
再生医学是一种再生医学.

背景情况:

衰老会使细胞外基质 (ECM) 变硬,阻碍肌肉的再生.
这种与年龄相关的ECM硬化通过不太了解的机制导致肌肉干细胞 (MuSC) 功能障碍.

研究的目的:

为了研究受ECM刚度影响的MuSC分化的与年龄相关的分子变化.
为了确定分子通路和转录因子驱动MuSC分化命运在不同的年龄和度条件下.

主要方法:

年轻和老的MuSCs在软硬的工程ECM基板上进行培养.
单细胞RNA测序 (scRNA) 用于分析分子变化.
使用β-aminopropionitrile (BAPN) 进行了体内原交联抑制.

主要成果:

从MuSC分化轨迹中出现了一个与年龄相关的纤维细胞群.
在硬基质上老化的细胞中观察到与TNF相关的诱导亡联体 (TRAIL) 途径的激活.
在老年动物中,BAPN治疗抑制了TRAIL下游的亡标,包括caspase 8和caspase 3.

结论:

随着年龄的增长,ECM 变硬会通过 TRAIL 路径的激活驱动 MuSC 功能障碍.
抑制ECM交叉链接部分逆转与年龄相关的TRAIL路径激活.
与年龄相关的肌肉功能下降涉及由ECM硬度影响的炎症和亡媒介.

关键词:

轨道的轨道是一个轨道.衰老的衰老衰老的衰老细胞外矩阵 (ECM) 是一个细胞外矩阵.纤维化转化为纤维化转化纤维化纤维化肌肉再生肌肉再生肌肉干细胞是肌肉的干细胞.scRNA分析 scRNA分析硬性硬性硬性

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