Transcriptome Signature of Cellular Senescence
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA541183 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9016150_1.fastq.gz | Fastqsanger.gz | |||
| SRR9016150_2.fastq.gz | Fastqsanger.gz | |||
| SRR9016160_1.fastq.gz | Fastqsanger.gz | |||
| SRR9016160_2.fastq.gz | Fastqsanger.gz | |||
| SRR9016170_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 74 |
Similar Datasets
Project description:Abstract: Cellular senescence, an integral component of aging and cancer, arises in response to diverse triggers, including telomere attrition, macromolecular damage, and signaling from activated oncogenes. At present, senescent cells are identified by the combined presence of multiple traits, such as senescence-associated protein expression and secretion, DNA damage, and β-galactosidase activity; unfortunately, these traits are neither exclusively nor universally present in senescent cells. To identify robust shared markers of senescence, we have performed RNA-sequencing analysis across 8 diverse models of senescence triggered in human diploid fibroblasts (WI-38, IMR-90) and endothelial cells (HUVEC, HAEC) by replicative exhaustion, exposure to ionizing radiation or doxorubicin, and expression of the oncogene HRASG12V. The intersection of the altered transcriptomes revealed 47 RNAs consistently elevated and 26 RNAs consistently reduced across all senescence models, including many protein-coding mRNAs and some long noncoding RNAs. We propose that these shared transcriptome profiles will enable the identification of senescent cells in vivo, the investigation of their roles in aging and malignancy, and the development of strategies to target senescent cells therapeutically.
2019-06-12 | GSE130727 | GEO
Project description:Cellular senescence, an integral component of aging and cancer, arises in response to diverse triggers, including telomere attrition, macromolecular damage and signaling from activated oncogenes. At present, senescent cells are identified by the combined presence of multiple traits, such as senescence-associated protein expression and secretion, DNA damage and β-galactosidase activity; unfortunately, these traits are neither exclusively nor universally present in senescent cells. To identify robust shared markers of senescence, we have performed RNA-sequencing analysis across eight diverse models of senescence triggered in human diploid fibroblasts (WI-38, IMR-90) and endothelial cells (HUVEC, HAEC) by replicative exhaustion, exposure to ionizing radiation or doxorubicin, and expression of the oncogene HRASG12V. The intersection of the altered transcriptomes revealed 50 RNAs consistently elevated and 18 RNAs consistently reduced across all senescence models, including many protein-coding mRNAs and some non-coding RNAs. We propose that these shared transcriptome profiles will enable the identification of senescent cells in vivo, the investigation of their roles in aging and malignancy and the development of strategies to target senescent cells therapeutically.
| S-EPMC6698740 | biostudies-literature
Project description:Cellular senescence, an irreversible proliferative arrest, functions in tissue remodeling during development and is implicated in multiple aging-associated diseases. While senescent cells often manifest an array of senescence-associated phenotypes, such as cell cycle arrest, altered heterochromatin architecture, reprogrammed metabolism and senescence-associated secretory phenotype(SASP), the identification of senescence cells has been hindered by lack of specific and universal biomarkers. To systematically identify universal biomarkers of cellular senescence, we integrated multiple transcriptome data sets of senescent cells obtained through different in vitro manipulation modes as well as age-related gene expression data of human tissues. Our analysis showed that RRAD (Ras-related associated with diabetes) expression is up-regulated in all the manipulation modes and increases with age in human skin and adipose tissues.
2018-11-20 | GSE116761 | GEO
Project description:The aim of the present study was to provide a comprehensive characterization of whole genome DNA methylation patterns in replicative and ionizing irradiation- or doxorubicin-induced premature senescence, exhaustively exploring epigenetic modifications in three different human cell types: in somatic diploid skin fibroblasts and in bone marrow- and adipose-derived mesenchymal stem cells. With CpG-wise differential analysis three epigenetic signatures were identified: a) cell type- and treatment-specific signature; b) cell type-specific senescence-related signature; and c) cell type-transversal replicative senescence-related signature. Cluster analysis revealed that only replicatively senescent cells created a distinct group reflecting notable alterations in the DNA methylation patterns accompanying this cellular state. Replicative senescence-associated epigenetic changes seemed to be of such an extent that they surpassed interpersonal dissimilarities. Enrichment in pathways linked to the nervous system and involved in the neurological functions was shown after pathway analysis of genes involved in the cell type-transversal replicative senescence-related signature. Although DNA methylation clock analysis provided no statistically significant evidence on epigenetic age acceleration related to senescence, a persistent trend of increased biological age in replicatively senescent cultures of all three cell types was observed. Overall, this work indicates the heterogeneity of senescent cells depending on the tissue of origin and the type of senescence inducer that could be putatively translated to a distinct impact on tissue homeostasis.
2023-03-20 | GSE227160 | GEO
Project description:Cellular proteostasis collapse in mammalian senescence
| PRJNA512837 | ENA
Project description:Pan-senescence transcriptome analysis identified RRAD as a marker and negative regulator of cellular senescence
| PRJNA480114 | ENA
Project description:RNA-seq was performed on early passage and senescent human retinal microvascular endothel cells (HRMECs), to determine transcriptomic changes. Replicative and Etoposide-induced senescent HRMECs senescence-associated gene signature and upregulation of an interferon related gene signature.
2023-10-27 | GSE160356 | GEO
Project description:In the present study we analyzed the effect of cellular senescence on the transcriptome of human mesenchymal stem cells (hMSC; alternatively named mesenchymal stromal cells) from bone marrow. Human MSC were isolated from femoral heads of non-osteoporotic donors after total hip arthroplasty. Cells were isolated from human bone marrow according to the previously described protocol (Noth et al., 2002, J Orthop Res, 20/5, 1060-1069) under agreement of the local Ethics Committee of the University of Würzburg. Bone marrow was obtained of femoral heads after total hip arthroplasty due to osteoarthritis and/or hip dysplasia. MSC were replated after reaching 70-90% confluence until they entered state of cellular senescence. RNA samples of control cells were taken from passage 1 or passage 2.
2012-02-22 | E-GEOD-35957 | biostudies-arrayexpress
Project description:Dermal cellular senescence model
2019-08-20 | 628 | FAIRDOMHub
Project description:ADAM19 Mediates Cellular Senescence and the Senescence-Associated Secretory Phenotype
2020-04-03 | MSV000085224 | MassIVE