Differential responses to aging amongst the transcriptome and proteome of mesenchymal progenitor populations.
Duque G., Feehan J., Tripodi N., Kondrikov D., Wijeratne T., Gimble J.
Laboratory Study on Systemic / IV, published in Res Sq (2023) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
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- Study type
- Laboratory Study
- Journal
- Res Sq (2023)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 38168272
- DOI
- 10.21203/rs.3.rs-3755129/v1
Abstract (original English)
Abstract The biological aging of mesenchymal stem cells is proposed to contribute to the development of a range of musculoskeletal and systemic diseases associated with older adults, such as osteoporosis, sarcopenia, and frailty. Despite this, little is understood about the specific mechanisms which drive this stem cell exhaustion, with most studies evaluating indirect effects of other aging changes, such as DNA damage, senescence, and inflammaging. In this study, we assess the transcriptomic and proteomic changes in three 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 males and females. These samples underwent RNA sequencing and label-free proteomic analysis, comparing the younger samples to the older ones. There was a distinct transcriptomic phenotype associated with the pooled older stem cells, indicative of suppressed proliferation and differentiation; however, there was no consistent change in the proteome of the cells. Older MPCs had a distinct phenotype in both the transcriptome and proteo
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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