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In-vivo Transcriptomic Profiling of Systemic Aging using Stem Cell Encapsulation

ABSTRACT: In-vivo Transcriptomic Profiling of Systemic Aging using Stem Cell Encapsulation

PROVIDER: PRJNA436920 | ENA |

REPOSITORIES: ENA

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In-vivo Transcriptomic Profiling of Systemic Aging using Stem Cell Encapsulation

Project description:Sustained exposure to a young systemic environment rejuvenates aged tissues and promotes stem cell function. However, due to the intrinsic complexity of tissues it remains challenging to pinpoint direct effects of circulating factors on specific cell populations. Here we describe a method for the encapsulation of human stem cells in highly diffusible polyethersulfone hollow fiber capsules that can be used to profile systemic aging independent of physical cellular interactions in-vivo.

2022-03-05 | GSE111401 | GEO

In Vivo Transcriptomic Profiling using Cell Encapsulation Identifies Effector Pathways of Systemic Aging

Project description:Sustained exposure to a young systemic environment rejuvenates aged organisms and promotes cellular function. However, due to the intrinsic complexity of tissues it remains challenging to pinpoint niche-independent effects of circulating factors on specific cell populations. Here we describe a method for the encapsulation of human and mouse skeletal muscle progenitors in diffusible polyethersulfone hollow fiber capsules that can be used to profile systemic aging in vivo independent of heterogeneous short-range tissue interactions. We observed that circulating long-range signaling factors in the old systemic environment lead to an activation of Myc and E2F transcription factors, induce senescence and suppress myogenic differentiation. Importantly, in vitro profiling using young and old serum in 2D culture does not capture all pathways deregulated in encapsulated cells in aged mice. Thus, in vivo transcriptomic profiling using cell encapsulation allows for the characterization of effector pathways of systemic aging with unparalleled accuracy.

2022-03-05 | GSE193665 | GEO

In Vivo Transcriptomic Profiling using Cell Encapsulation Identifies Effector Pathways of Systemic Aging

Project description:In Vivo Transcriptomic Profiling using Cell Encapsulation Identifies Effector Pathways of Systemic Aging

| PRJNA797090 | ENA

In vivo transcriptomic profiling using cell encapsulation identifies effector pathways of systemic aging.

Project description: Not available

| S-EPMC8926399 | biostudies-literature

Endothelial C/EBPβ/AEP Pathway Drives Vascular Deterioration and Systemic Aging

Project description:Age-related microvascular dysfunction disrupts nutrient homeostasis and waste clearance, leading to organ failure. However, a critical gap remains in our understanding of the specific molecular drivers of vascular deterioration and how they orchestrate organism-wide aging. Here, we identify progressive activation of the CCAAT/enhancer-binding protein β (C/EBPβ)/asparagine endopeptidase (AEP) pathway in aging vascular endothelial cells contributes to vascular degeneration and lifespan reduction. Endothelial-specific C/EBPβ or AEP overexpression accelerated vascular aging and shortened lifespan in mice. Mechanistically, AEP mediates proteolytic cleavage of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in nicotinamide adenine dinucleotide (oxidised form, NAD+) biosynthesis, resulting in systemic NAD⁺ depletion and senescence that elicits both central and peripheral vascular dysfunction and ultimately systemic aging. Genetic ablation of AEP or expression of AEP-resistant NAMPT N136A mutant significantly ameliorated vascular aging and extended lifespan in endothelial-specific Tie 2-C/EBPβ transgenic mice. Pharmacologically, AEP inhibitor CP#11A or nicotinamide mononucleotide (NMN) supplementation alleviated age-related vascular decline, with CP#11A showing superior efficacy. These findings support a model in which endothelial senescence contributes to vascular dysfunction and systemic aging mediated by C/EBPβ/AEP signaling, and establish C/EBPβ/AEP as a therapeutic target to preserve vascular integrity and mitigate systemic frailty in aging populations.

2026-05-30 | E-MTAB-17006 | biostudies-arrayexpress

HuR coordinates systemic aging through platelet infiltration.

Project description:HuR coordinates systemic aging through platelet infiltration.

| PRJNA1298823 | ENA

HuR coordinates systemic aging through platelet infiltration

Project description:HuR coordinates systemic aging through platelet infiltration

| PRJNA1184739 | ENA

Menopause transition timing reflects systemic biological aging

Project description:Menopause transition timing reflects systemic biological aging

| PRJNA1493061 | ENA

HuR coordinates systemic aging through platelet infiltration.

Project description:Aging involves morphological and functional changes across different organs, but how these changes are linked among the different organs remains to be elucidated. Here, we uncover a central role of platelets in systemic aging. In aged mice, the levels of platelet-secreted pro-inflammatory factors (PSPF) increased greatly in the serum and platelets, leading to a diffuse increase of platelet infiltration in brain, liver, lung, kidney, and aortic root. The RNA-binding protein HuR/ELAVL1, a major regulator of RNA metabolism, promoted the production of PSPF in platelets. Platelet-specific deletion of HuR reduced the expression of PSPF in platelets, alleviated platelet infiltration in brain, liver, lung, kidney, and aortic root, and delayed systemic aging. By using single-nucleus sequencing, platelet-specific HuR ablation was found to alleviate p53 and pro-inflammatory signaling pathways in liver, lung, and brain tissues in aged mice. Our findings highlight a role of platelets in coordinating aging traits across organs.

2026-07-22 | GSE304047 | GEO

A Virus-acquired Host Cytokine Controls Systemic Aging by Antagonizing Apoptosis

Project description:Aging is characterized by degeneration of unique tissues. However, dissecting the interconnectedness of tissue aging remains a challenge. Here, we employ a muscle-specific DNA damage model in Drosophila to reveal secreted factors that influence systemic aging in distal tissues. Utilizing this model, we uncovered a cytokine, Diedel, that when secreted from muscle or adipose can attenuate age-related intestinal tissue degeneration by promoting proliferative homeostasis of stem cells. Diedel is both necessary and sufficient to limit tissue degeneration and extend lifespan. Secreted homologs of Diedel are also found in viruses, having been acquired from host genomes. Focusing on potential mechanistic overlap between cellular aging and viral-host cell interactions and, we found that Diedel is a functionally conserved inhibitor of apoptosis and can act as a systemic rheostat to modulate cell death during aging. These results highlight a key role for secreted antagonists of apoptosis in the systemic coordination of tissue aging.

2018-07-02 | GSE111248 | GEO

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