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在衰老过程中,脂肪组织中中介细胞干细胞异质性的融合变化

Qiwei Liu^1,2, Yu Zhao^1,2, Qian Wang^1,2

¹Research Center of Plastic Surgery Hospital, Chinese Academy of Medical Science & Peking Union Medical College, Beijing, P. R. China.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

|July 27, 2023

概括

衰老导致脂肪衍生干细胞 (ASC) 失去异质性,ASC亚型4主导和分化. 炎症因子CCL2和CCL7驱动这些与年龄相关的ASC变化.

科学领域:

干细胞生物学干细胞生物学
衰老研究研究衰老研究
脂肪组织生物学脂肪组织生物学

背景情况:

脂肪系干细胞 (ASC) 具有年龄相关的特征,但其异质性随着年龄的增长而变化并未得到充分理解.
了解ASC衰老对于再生医学和治疗应用至关重要.

研究的目的:

通过单细胞RNA测序来研究ASC异质性的年龄相关变化.
确定ASC衰老和分化的关键分子驱动因素.

主要方法:

对公开可用的单细胞RNA测序数据的分析,这些数据来自不同年龄组 (年轻人,成年人,老年人) 的小鼠 inguinal 脂肪组织.
转录组聚类,调节子分析和配体-受体相互作用分析.
在体外实验评估CCL2和CCL7对ASC的影响.

主要成果:

确定了五种ASC亚型,老化导致ASC亚型4 (ASC-4) 的异质性和主导性显著丧失.
随着年龄的增长,ASC-4表现出增加的脂肪生成潜力,由转录因子Cebpb驱动.
观察到与年龄相关的炎症因子CCL2和CCL7的上调,CCL2促进脂肪生成,CCL7可能导致ASC的趋同.

结论:

衰老显著改变ASC异质性,导致主导的,终端差异化的ASC-4亚群.
炎症因子CCL2和CCL7在调解与年龄相关的ASC变化方面发挥着关键作用.
这些发现提供了关于ASC衰老机制和潜在治疗点的见解.

关键词:

脂肪衍生干细胞来源的干细胞.老化的老化衰老的老化异质性的异质性一个单细胞RNA测序.

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