Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GNPS - Exosomes Released from Senescent Cells and Isolated from Human Plasma Reveal Aging-associated Proteomic Signatures

ABSTRACT: Senescence emerged as a significant mechanism of aging and age-related diseases, offering an attractive target for clinical intervention. Senescent cells release senescence-associated secretory phenotype (SASP), including exosomes that may act as signal transducers between distal tissues, propagating secondary senescence and signaling throughout the body. However, the composition of exosome SASP remains underexplored, presenting an opportunity for novel unbiased discovery. Here, we present a detailed lipidomic analysis of exosome SASP using mass spectrometry from senescent primary human lung fibroblasts and human plasma from young and older individuals.

INSTRUMENT(S): 6560 Q-TOF LC/MS

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Erin Baker

PROVIDER: MSV000094326 | GNPS | Fri Mar 15 06:28:00 GMT 2024

REPOSITORIES: GNPS

ACCESS DATA

Json Xml

Similar Datasets

Exosomes Released from Senescent Cells and Isolated from Human Plasma Reveal Aging-associated Proteomic Signatures

Project description:Senescence emerged as a significant mechanism of aging and age-related diseases, offering an attractive target for clinical intervention. Senescent cells release senescence-associated secretory phenotype (SASP), including exosomes that may act as signal transducers between distal tissues, propagating secondary senescence and signaling throughout the body. However, the composition of exosome SASP remains underexplored, presenting an opportunity for novel unbiased discovery. Here, we present a detailed lipidomic analysis of exosome SASP using mass spectrometry from senescent primary human lung fibroblasts and human plasma from young and older individuals.

2024-03-15 | MSV000094326 | MassIVE

The effects of mitochondrial damages under stress or during aging on osteocytes networks homeostasis

Project description:Using oligomycin A-treated MLO-Y4 cells and primary murine aging osteocytes as a model of cells with mitochondrial dysfunction, it is demonstrated that when mitochondria are damaged, osteocytes tend to release signaling compounds including adenosine diphosphate. We identified that the nucleotide membrane receptors P2Y2 and P2Y6 transduced the ADP signal to Mfn2, a critical regulator of osteocyte mitochondrial transfer. Whole RNA sequencing (RNA-seq) analysis of mouse cortical bone showed that mitochondrial metabolism is impaired in aged osteocytes, and there are more extracellular nucleotides released into the matrix in cortical bone in aged mice as compared to that in young mice. Aging decreases expression levels of P2Y2/P2Y6 and Mfn2.

2024-01-24 | GSE235103 | GEO

Gene Microarrays in Hippocampal Aging

Project description:Male Fischer 344 rats aged 4 months (young, n=10), 14 months (mid-aged, n=10), and 24 months (aged, n=10) were trained sequentially on two tasks: Morris Spatial Water Maze (SWM) and Object Memory Task (OMT). The training/testing sequence lasted 7 d, and hippocampal tissue was collected 24 hr later. Training and testing occured on each day except for days 2 and 3 of the 7 d sequence. (01/10/05: Series was updated to correct mislabeling of all sample signal values within the Young Treatment Group) Keywords = bioinformatics Keywords = gene expression Keywords = memory Keywords = synaptic plasticity Keywords = myelin Keywords = inflamation Keywords = aging Keywords: repeat sample

2005-01-10 | GSE854 | GEO

Directly Reprogrammed Human Neurons Retain Aging-Associated Transcriptomic Signatures and Reveal Age-Related Nucleocytoplasmic Defects.

Project description: Not available

| S-EPMC5929130 | biostudies-literature

Repertoire-wide phylogenetic models of B cell molecular evolution reveal evolutionary signatures of aging and vaccination.

Project description: Not available

| S-EPMC6842591 | biostudies-literature

Single-cell transcriptomes of the aging human skin reveal loss of fibroblast priming

Project description:Fibroblasts are the main dermal cell type and are essential for the architecture and function of human skin. Important differences have been described between fibroblasts localized in distinct dermal layers, and these cells are also known to perform varied functions. However, this phenomenon has not been analyzed comprehensively yet. Here we have used single-cell RNA sequencing to analyze >15,000 cells from a sun-protected area in young and old donors. Our results define four main fibroblast subpopulations that can be spatially localized and functionally distinguished. Importantly, intrinsic aging reduces this fibroblast ‘priming’, generates distinct expression patterns of skin aging-associated genes, and substantially reduces the interactions of dermal fibroblasts with other skin cell types. Our work thus provides comprehensive evidence for a functional specialization of human dermal fibroblasts and suggests that the age-related loss of fibroblast priming contributes to human skin aging.

2020-03-31 | GSE130973 | GEO

Biomarker signatures of aging.

Project description: Not available

| S-EPMC5334528 | biostudies-literature

Multi-Omics Analyses Revealed Conserved Aging Signatures in Mice

Project description:Studies on aging have largely included one or two OMICS layers, which may not necessarily reflect the signatures of other layers. Moreover, most aging studies have often compared very young (4-5 wks) mice with old (24 months) mice which does not reflect the aging transition after the attainment of adulthood. Therefore, we aimed to study and compared muti-OMICS aging signatures across key metabolic tissues of mature adults (6 months) and old (24 months) C57BL/6J mice (the most commonly used mouse strain). Here we compared the differentially regulated genes and enriched pathways for transcriptome, proteome and epigenome (H3K27ac, H3K4me3, H3K27me3, DNA methylation) across liver, heart, and quadriceps muscle. The major aging associated pathways cross multiple layers and tissues are decreased RNA metabolism, transcription, and translation at transcript and protein levels however increased potential of transcription at DNA methylation and H3K27ac levels.

2021-11-30 | PXD011142 | Pride

Epigenome analysis of aging muscle progenitors

Project description:Genome wide DNA methylation profiling of muscle cells extracted from healthy donors at different ages. The Illumina Infinium Human Methylation 450 BeadChip was used to obtain DNA methylation profiles across > 485,000 methylation sites. The muscle cells were extracted from young adults (18-40 years old) and elderly (>70 years old)(n=3 per group, 2 groups : Young and aged adult). Bisulphite converted DNA from the 6 samples were hybridized to the Illumina Infinium Human Methylation 450 BeadChip

2015-05-01 | E-GEOD-53302 | biostudies-arrayexpress

Transcriptomic analysis of mouse brain microglia on aging-associated changes in response to cerebral ischemia

Project description:Senescence-associated alterations in microglia may have profound impact on cerebral homeostasis and stroke outcomes. However, the lack of a transcriptome-wide comparison between young and aged microglia in the context of ischemia limits our understanding of aging-related mechanisms. Herein, we performed bulk RNA sequencing analysis of microglia purified from cerebral hemispheres of young adult (10-week-old) and aged (18-month-old) mice 5 days after distal middle cerebral artery occlusion or sham operation. Considerable transcriptional differences were observed between young and aged microglia in healthy brains, indicating heightened chronic inflammation in aged microglia. Following stroke, the overall transcriptional activation was more robust in young microglia than in aged microglia. Gene clusters with functional implications in immune inflammatory responses, immune cell chemotaxis, tissue remodeling, and cell-cell interactions were markedly activated in microglia of young but not aged stroke mice. These alterations in microglial gene response may contribute to aging-driven vulnerability and poorer recovery after ischemic stroke.

2020-05-31 | GSE145265 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data