间充质祖细胞转录组和蛋白质组对衰老的不同反应。

Jack Feehan, Nicholas Tripodi, Dmitry Kondrikov, Tissa Wijeratne, Jeffrey Gimble, William Hill, Vasso Apostolopoulos, Gustavo Duque
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引用次数: 0

摘要

干细胞的生物衰老(衰竭)被认为是导致各种年龄相关疾病的原因。尽管如此,人们对驱动这一过程的具体机制知之甚少。在本研究中,我们评估了来自老年人(50-70岁)和年轻人(20-40岁)的间充质祖细胞三个不同群体的转录组和蛋白质组变化,以揭示间充质组织中驱动干细胞衰竭的潜在机制。为此,我们从年轻和年长的捐献者身上采集了原始骨髓间充质干细胞和祖细胞(MPCs)、循环造骨细胞(COP)和脂肪来源干细胞(ADSCs),其中男性和女性样本的数量相等。对这些样本进行了 RNA 测序和无标记蛋白质组分析,并将年轻样本与年长样本进行了比较。在对汇集的老年干细胞进行分析时,发现了一种独特的转录组表型,表明增殖和分化受到抑制;但这些变化并没有反映在细胞的蛋白质组中。通过独立分析,老年多核干细胞在转录组和蛋白质组中都有不同的表型,这与分化和增殖的改变一致,表明老年人的免疫系统发生了促炎性转变。COP 细胞显示转录组向促炎信号转变,但没有一致的蛋白质组表型。同样,ADSCs 在与细胞迁移、粘附和免疫激活相关的生理过程中显示出转录组变化,但蛋白质组没有随着年龄的增长而变化。这些结果表明,干细胞衰老会引起潜在的转录组变化,可能导致组织再生能力下降。然而,细胞蛋白质组的调控却不一致。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Differential Responses to Aging Among the Transcriptome and Proteome of Mesenchymal Progenitor Populations.

The biological aging of stem cells (exhaustion) is proposed to contribute to the development of a variety of age-related conditions. Despite this, little is understood about the specific mechanisms which drive this process. In this study, we assess the transcriptomic and proteomic changes in 3 different populations of mesenchymal progenitor cells from older (50-70 years) and younger (20-40 years) individuals to uncover potential mechanisms driving stem cell exhaustion in mesenchymal tissues. To do this, we harvested primary bone marrow mesenchymal stem and progenitor cells (MPCs), circulating osteoprogenitors (COP), and adipose-derived stem cells (ADSCs) from younger and older donors, with an equal number of samples from men and women. These samples underwent RNA sequencing and label-free proteomic analysis, comparing the younger samples to the older ones. There was a distinct transcriptomic phenotype in the analysis of pooled older stem cells, suggestive of suppressed proliferation and differentiation; however, these changes were not reflected in the proteome of the cells. Analyzed independently, older MPCs had a distinct phenotype in both the transcriptome and proteome consistent with altered differentiation and proliferation with a proinflammatory immune shift in older adults. COP cells showed a transcriptomic shift to proinflammatory signaling but no consistent proteomic phenotype. Similarly, ADSCs displayed transcriptomic shifts in physiologies associated with cell migration, adherence, and immune activation but no proteomic change with age. These results show that there are underlying transcriptomic changes with stem cell aging that may contribute to a decline in tissue regeneration. However, the proteome of the cells was inconsistently regulated.

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