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GDF11和TET2之间的相互调节可以防止中酶体干细胞的衰老

Jiaming Gao¹, Hao Wang¹, Junyan Shen¹

¹Institute for Regenerative Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.

Journal of cellular physiology

|October 6, 2023

概括

增长分化因子11 (GDF11) 通过激活关键通路和上调DNA脱甲基酶Tet2.2,使衰老的介质干细胞 (MSCs) 复苏. 这建立了一个新的反循环,对于维持细胞的年轻和功能至关重要.

科学领域:

细胞生物学细胞生物学
分子生物学分子生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

衰老的介质干细胞 (MSCs) 呈现出减少的增殖,衰老标志物和削弱的骨质生成潜力.
增长区分因子11 (GDF11) 被认为是一种具有潜在抗衰老特性的系统性因子.
了解GDF11在MSC衰老中的分子机制对于再生医学至关重要.

研究的目的:

阐明GDF11在介质干细胞 (MSC) 中逆转衰老的机制.
研究GDF11在调节细胞衰老和干细胞功能中的作用.
确定涉及GDF11介导的抗衰老效应的新型分子通路.

主要方法:

关于增殖,衰老标志物 (β-galactosidase,P16^ink4a),端粒长度,GDF11表达和骨质生成潜力的老年MSC的表征.
在体外和体内实验中评估GDF11对MSC衰老和骨质损失的影响.
通过GDF11.11对Smad2/3-PI3K-AKT-mTOR通路激活的分析.
研究GDF11与DNA脱甲基酶Tet2的相互作用及其对GDF11促进剂甲基化的影响.

主要成果:

在实验室中,GDF11治疗阻断了MSC的衰老,并在体内逆转了因年龄而导致的骨质损失.
通过激活Smad2/3-PI3K-AKT-mTOR通路,GDF11的抗衰老作用受到介导.
GDF11上调调节了Tet2,一种通过促进物脱甲基化自调节GDF11表达的DNA脱甲基酶.
Tet2 缺乏或 Tet2 调节的 CpG 位点的突变发生会损害 GDF11 表达,加速 MSC 的衰老.

结论:

GDF11有效地逆转MSC衰老,并通过特定的分子通路改善干细胞功能.
在GDF11和表观遗传因子Tet2之间存在一种新的相互调节关系,突出了它们的联合抗衰老作用.
这项研究揭示了一种关键的表观遗传机制,涉及Tet2在GDF11介导的青春期,为与年龄相关的衰退提供了潜在的治疗点.

关键词:

在TET2的基础上.细胞衰老细胞衰老介质细胞干细胞介质细胞干细胞

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