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Extracellular vesicles from antler blastema progenitor cells reverse bone loss and improve aging-related phenotypes in mice and macaques [RNA-seq]

ABSTRACT: Antler blastema progenitor cell (ABPC) is a novel type of skeletal mesenchymal stem cell with strong stemness and renewal ability. Here, we discovered that ABPC-derived extracellular vesicles (EVsABPCs) can strongly rejuvenate aging tissues in aged mice and rhesus macaques (Macaca mulattas). We identified a variety of rejuvenating molecules in EVsABPCs that differed from EVs of mouse bone marrow stromal stem cells (EVsBMSCs). EVsABPCs exhibited a robust in vitro ability to rejuvenate senescence BMSCs of aged mice and shift their molecular signature into a youthful state. In vivo, EVsABPCs increased bone mineral density in the femur by 2.4-fold in mice, and 1.53-fold in rhesus macaques. Besides, intravenous EVsABPCs significantly outperformed mouse fetal-EVsBMSCs in improving physical performance, reducing systemic inflammation, and rejuvenating major tissues of elderly mice, with no observed immunological side effects. Furthermore, EVsABPCs showed similar rejuvenating effects in old rhesus macaques as in elderly mice. Particularly, EVsABPCs resulted in remarkable improvements in brain structure and behaviors of elderly rhesus macaques, providing the first batch of evidence of EVs’ beneficial effects on aging brains in primates. These findings suggest that the ABPC is a novel and practical source of EVs containing a wealth of systemic rejuvenating factors and has considerable translational value for anti-aging interventions, particularly the rejuvenation of aging bones.

ORGANISM(S): Mus musculus Rattus norvegicus

PROVIDER: GSE289038 | GEO | 2025/05/13

REPOSITORIES: GEO

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Project description:Extracellular vesicles (EVs) have several functions in the brain, serving as a mode of intercellular communication and as a pathway for disposal of cellular debris. While these functions serve to maintain healthy brain function, they may also contribute to diseases affecting the brain. EVs also change with aging of the brain, as levels of some EV subtypes increase at advanced ages in mice. These changes could be caused by aging-related changes such as inflammation, cellular senescence, or impairment of autophagy or mitochondrial function. Aging-related changes in brain EVs might also further aging-related changes, as levels of EVs in plasma may change with age and contribute to aging-related changes in inflammation and cellular metabolism. However, the effects of aging on brain EVs and the potential contribution of EVs to aging-related changes in the brain are not well understood. To address this question, we investigated the levels and protein contents of EVs isolated from brains of 4-, 12-, and 22-month–old C57Bl/6J mice. We detected no changes in EV levels, but observed age-dependent changes in EV proteins. EV fractions from aged (22-month–old) mice contained higher levels of extracellular matrix proteins than EV fractions from young (4-month–old) mice, with similar trends occurring in 12-month–old mice. Specifically, levels of hyaluronan and proteoglycan link proteins (Hapln) 1 and 2 were elevated in EV fractions from aged mice, as were levels of several chondroitin sulfate proteoglycans (CSPGs), which interact with Hapln1 and 2. Analysis of extracellular matrix in several brain regions of aged mice revealed increased immunolabeling for aggrecan, but an overall reduction in labeling with Wisteria floribunda agglutinin, which binds to chondroitin sulfate. These data are consistent with prior studies showing changes to the composition of extracellular matrix in aged brains, which might contribute to age-related cognitive decline. These findings reveal a novel association of EVs with changes in the extracellular matrix of the aging brain.

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Extracellular vesicles from antler blastema progenitor cells reverse bone loss and improve aging-related phenotypes in mice and macaques [RNA-seq]

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