Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SenCat: Cataloging human cell senescence through multiomic profiling of multiple senescent primary cell types

ABSTRACT: There is an urgent need to comprehensively catalog senescence markers across a wide range of cell types in an organism. Here, we profiled the transcriptomes and proteomes in over 30 senescence paradigms employing 14 different primary human cell types. Our results indicate that senescent cells from all tissue types do not share a unique marker, but they do share in the activation of specific metabolic pathways and damage response pathways to elicit tissue repair. Importantly, considering combinations of some of the most widely shared senescence markers validated the presence of senescent-like cells in mice through single-cell RNA-sequencing and immunostaining approaches. The enclosed catalog represents a much-needed resource to identify senescent cells across tissues in the body.

ORGANISM(S): Mus musculus

PROVIDER: GSE302792 | GEO | 2026/06/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

SenCat: Redefining human cell senescence through multiomic profiling of multiple senescent cell types

Project description:There is an urgent need to comprehensively catalog senescence markers across a wide range of cell types in an organism. Here, we profiled the transcriptomes and proteomes in over 30 senescence paradigms employing 14 different primary human cell types. Our results indicate that senescent cells from all tissue types do not share a unique marker, but they do share in the activation of specific metabolic pathways and damage response pathways to elicit tissue repair. Importantly, considering combinations of some of the most widely shared senescence markers validated the presence of senescent-like cells in mice through single-cell RNA-sequencing and immunostaining approaches. The enclosed catalog represents a much-needed resource to identify senescent cells across tissues in the body.

2026-06-15 | GSE284666 | GEO

SenCat: Redefining human cell senescence through multiomic profiling of multiple senescent cell types [scRNA-seq]

2026-06-15 | GSE285108 | GEO

SenCat: Redefining human cell senescence through multiomic profiling of multiple senescent cell types

Project description:There is an urgent need to comprehensively catalog senescence markers across the wide range of cell types in an organism. Here, we profiled the transcriptomes and proteomes of over 30 models of senescence in 14 different primary human cell types. We found that senescent cells from all tissue types do not share a unique marker, but they do share broadly activated or repressed pathways, namely pathways of damage response to elicit tissue repair, and unique metabolic pathways. Importantly, the combined use of some of the most widely shared senescence markers validated the presence of senescent-like cells in mice through single-cell RNA-sequencing and immunostaining approaches. The enclosed catalog represents a much-needed resource to identify senescent cells across tissues in the body.

2024-10-25 | MSV000096215 | MassIVE

SenCat: Redefining human cell senescence through multiomic profiling of multiple senescent cell types

Project description:SenCat: Redefining human cell senescence through multiomic profiling of multiple senescent cell types

| PRJNA1200021 | ENA

SenCat: Cataloging human cell senescence through multiomic profiling of multiple senescent primary cell types

Project description:SenCat: Cataloging human cell senescence through multiomic profiling of multiple senescent primary cell types

| PRJNA1292169 | ENA

Senescent and myofibroblastic cancer-associated fibroblasts share a contractile phenotype regulated by NOX4 generation of reactive oxygen species in the tumour microenvironment

Project description:Cancer associated fibroblasts characterized by an myofibroblastic phenotype play a major role in the tumour microenvironment, being associated with poor prognosis. We found that this cell population is made in part by senescent fibroblasts in vivo. As senescent fibroblasts and myofibroblasts have been shown to share similar tumour promoting functions in vitro we compared the transcriptosomes of these two fibroblast types and performed RNA-seq of human foetal foreskin fibroblasts 2 (HFFF2) treated with 2ng/ml TGF-beta-1 to induce myofibroblast differentiation or 10Gy gamma irradiation to induce senescence. We isolated RNA 7 days upon this treatments changing the medium 3 days before the RNA extraction. A series of SAM alignment files (named after the sample names, for simplicity) are available under http://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-3101/files/ .

2017-06-01 | E-MTAB-3101 | biostudies-arrayexpress

Primary oocytes with cellular senescence features are involved in ovarian aging in mice

Project description:In mammalian females, quiescent primordial follicles serve as the ovarian reserve and sustain normal ovarian function and egg production via folliculogenesis. The loss of primordial follicles causes ovarian aging. Cellular senescence, characterized by cell cycle arrest and production of the senescence-associated secretory phenotype (SASP), is associated with tissue aging. In the present study, we report that some quiescent primary oocytes in primordial follicles become senescent in adult mouse ovaries. The senescent primary oocytes share senescence markers characterized in senescent somatic cells. The senescent primary oocytes were observed in young adult mouse ovaries, remained at approximately 15% of the total primary oocytes during ovarian aging from 6 months to 12 months, and accumulated in aged ovaries. Administration of a senolytic drug ABT263 to 3-month-old mice reduced the percentage of senescent primary oocytes and the transcription of the SASP cytokines in the ovary. In addition, led to increased numbers of primordial and total follicles and a higher rate of oocyte maturation and female fertility. Our study provides experimental evidence that primary oocytes, a germline cell type that is arrested in meiosis, become senescent in adult mouse ovaries and that senescent cell clearance reduced primordial follicle loss and mitigated ovarian aging phenotypes.

2024-04-30 | GSE253194 | GEO

Cellular senescence escape and antiviral response discriminate glioblastoma from lower grade gliomas

Project description:Cellular senescence is a negative prognostic indicator in glioblastoma (GB). However, the specific cell types exhibiting senescence and the molecular mechanisms by which senescent cells (SCs) contribute to GB pathogenesis remain unknown. We performed multi-omics integration of publicly available GB patient-derived datasets to identify SCs and their functional impact on GB pathogenesis. We created a transcriptomic definition of SCs to verify their presence in GB datasets. Next, we analyzed transcriptomic profiles of GB and low-grade gliomas to reveal key features of GB aggressiveness. The GB patients’ phosphoproteome was analyzed with a focus on key regulators of senescence. To assess chemotherapy-evoked secondary senescence, we performed a proteomic analysis of temozolomide-induced senescence in human GB spheroids. We identified GB-associated SCs in clusters radial glia, endothelial cells, and immature astrocytes localized primarily in the hypoxic zones. Notably, we identified senescence-escape features and tumor antiviral responses as processes distinguishing GB from low-grade gliomas. In GB samples, we detected inhibitory phosphorylation of p21 and p27 proteins and active PI3K signaling, which can lead to senescence escape and belong to the typical manipulation arsenal of herpesviruses. Our proteomic analysis of temozolomide-induced senescent GB cells reveals that primary (pre-radiochemotherapy) and secondary senescence in GB share similar phenotypic features. Pathways associated with GB aggressiveness are upregulated after therapy, which can promote more aggressive behavior of recurrent tumors. Our data indicate that senescence and viral reactivation may fuel GB progression, including recurrence, suggesting that senolytics and antiviral drugs are potential therapeutic avenues.

2026-06-08 | PXD071225 | Pride

Potential roles of DNA methylation in the initiation and establishment of replicative senescence revealed by array-based methylome and transcriptome analyses [methylation 450K]

Project description:Cellular senescence is classified into two types; replicative and premature senescence. Gene expression and epigenetic changes are different in types of senescence, replicative and premature senescence, and cell types. Normal human diploid fibroblast TIG-3 cells were often used in cellular senescence research, however, their epigenetic profiles were not fully understood. To elucidate how cellular senescence is epigenetically regulated in TIG-3 cells, we analyzed gene expression and DNA methylation profiles among three types of senescent cells, namely, replicative senescent, RAS-induced senescent (RIS) and non-permissive temperature-induced senescent SVts8 cells, using gene expression and methylation microarrays. The expression of genes involved in cell cycle and immune response were commonly either down- or up-regulated among three types of senescent cells, respectively. The sequential alteration of DNA methylation level was observed only in replicative senescent cells in a time-dependent manner, but not in premature senescent cells. The integrated analysis of gene expression and methylation in replicative senescent cells demonstrated that the expression of 759 genes involved in cell cycle and immune response was associated with methylation. Furthermore, hypomethylation occurred at non-CpG island regions (open sea) on the genes with increased expression as well as non-CpG promoter of the genes related to immune response. Several miRNAs regulated by DNA methylation were found to affect the expression of their target genes. Taken together, these results indicate that DNA methylation contributes to introduction and establishment of replicative senescence partly by regulating gene expression.

2017-02-12 | GSE81797 | GEO

Potential roles of DNA methylation in the initiation and establishment of replicative senescence revealed by array-based methylome and transcriptome analyses [expression]

2017-02-12 | GSE81786 | GEO