Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human vascular smooth muscle cells undergoing cell senescence

ABSTRACT: Vascular smooth muscle cells (VSMCs) undergo cell senescence in a number of diseases, both due to stress and loss of replication. Here we have cultured human VSMCs to replicative senescence, or induced stress-induced premature senescence (SIPS), and compared their transcriptome with cells treated with doxorubicin for 1d or control cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE171663 | GEO | 2021/05/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Increased vascular smooth muscle cell senescence in aneurysmal Fibulin-4 mutant mice

Project description:Aortic aneurysms are dilations of the aorta that can rupture when left untreated. We used aneurysmal Fibulin-4R/R to further unravel the underlying mechanisms of aneurysm formation. RNA sequencing of 3-month-old Fibulin-4R/R aortas revealed significant upregulation of senescence-associated secretory phenotype (SASP) factors and key senescence factors, indicating involvement of senescence. Analysis of aorta histology and of vascular smooth muscle cells (VSMCs) in vitro confirmed the senescent phenotype of Fibulin-4R/R VSMCs by revealing increased SA-β-gal, p21 and p16 staining, increased IL-6 secretion, increased presence of DNA damage foci and increased nuclei size. Additionally, we found that p21 luminescence was increased in the dilated aorta of Fibulin-4R/R|p21-Luciferase mice. Our studies identify a cellular aging cascade in Fibulin-4 aneurysmal disease, by revealing that Fibulin-4R/R aortic VSMCs have a pronounced SASP and a senescent phenotype that may underlie aortic wall degeneration. Additionally, we demonstrated the therapeutic effect of JAK/STAT and TGF-β pathway inhibition as well as senolytic treatment on Fibulin-4R/R VSMCs in vitro. These findings can contribute to improved therapeutic options for aneurysmal disease aimed at reducing senescent cells.

2024-04-30 | GSE265869 | GEO

Human vascular smooth muscle cells undergoing cell senescence

Project description:Human vascular smooth muscle cells undergoing cell senescence

| PRJNA720431 | ENA

Human primary fetal lung fibroblasts (HFL-1) undergoing replicative senescence

Project description:We profiled the global gene expression of human primary fetal lung fibroblasts (HFL-1) at different stages while they were undergoing replicative senescence

2020-08-10 | GSE144703 | GEO

Vascular smooth muscle cell senescence instigates thoracic aortic aneurysm

Project description:In this study, we identified various cell clusters in human normal/sporadic TAA ascending aorta samples by single-cell RNA sequencing (scRNA-seq), and discovered the senescent vascular smooth muscle cells (VSMCs) significantly increased in TAA samples. Then we explored the molecular basis of TAA progression, and recognized the key regulators and pathways involved in the TAA progression regulation.

2023-12-01 | GSE143921 | GEO

DNA methylation analysis of cellular senescence

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

Senescence-specific gene expression fingerprints

Project description:This SuperSeries is composed of the following subset Series: GSE3730: Replicative senescence in human fibroblasts GSE3731: Replicative senescence in post-selection HMECs Abstract: Replicative senescence is the state of irreversible proliferative arrest that occurs as a concomitant of progressive telomere shortening. By using cDNA microarrays and the gabriel system of computer programs to apply domain-specific and procedural knowledge for data analysis, we investigated global changes in gene transcription occurring during replicative senescence in human fibroblasts and mammary epithelial cells (HMECs). Here we report the identification of transcriptional "fingerprints" unique to senescence, the finding that gene expression perturbations during senescence differ greatly in fibroblasts and HMECs, and the discovery that despite the disparate nature of the chromosomal loci affected by senescence in fibroblasts and HMECs, the up-regulated loci in both types of cells show physical clustering. This clustering, which contrasts with the random distribution of genes down-regulated during senescence or up-regulated during reversible proliferative arrest (i.e., quiescence), supports the view that replicative senescence is associated with alteration of chromatin structure. Refer to individual Series

2006-03-06 | E-GEOD-4352 | biostudies-arrayexpress

RNAseq of Normal Human Epidermal Keratinocytes (NHEKs) in UVB-induced senescence (UVB-SIPS, at 3 days or 5 days) or in replicative-like senescence (RS)

Project description:RNAseq analyses of NHEKs in replicative-like senescence, i.e. in growth arrest after about ten passages in culture, or in premature senescence induced by repeated UVB exposures (UVB-SIPS), at 3 days and at 5 days after the last UVB stress.

2022-12-31 | E-MTAB-10969 | biostudies-arrayexpress

Disfunction of arachidonic acid metabolism in vascular smooth muscle cells contributes to restenosis

Project description:We applied the transcriptome profiling (RNA-seq) for high-throughput profiling of genes changes in the phenotypic switch of VSMCs. Rat primary VSMCs were divided into 3 groups, control, PDGF-BB, PDGF-BB+PTUPB,and mRNA sequence were performed. We found that Cell cycle related genes and cellular senescence related genes were significantly upregulated by PDGF-BB and significantly reversed by PTUPB. Subsequently, we deleted PTTG1 as a key gene for PTUPB to reverse phenotypic switching in VSMCs. Our study provided the transcription changes by RNA-seq in VSMC phenotypic switch, and found that PTUPB played a crucial role in correcting the dysregulation of sEH/COX-2 derived ARA metabolism in VSMC phenotypic switch

2023-09-01 | GSE241545 | GEO

Stretch-dependent genes in vascular smooth muscle cells

Project description:Vascular smooth muscle cells (VSMCs) respond to biomechanical stretch with specific changes in gene expression which govern the phenotype of these cells. The mechanotransducer zyxin is a potential candidate for regulating the expression of such genes. Using microarrays, we compared stretch-induced gene expression in wild type and zyxin-null VSMCs to define such changes in detail. Wild type (WT) and zyxin-null VSMCs were stretched at 10% cyclic elongation for 6 hours and the changes in gene expression were compared under static and stretched conditions. Up to 3 biological replicates were used for each of the 4 sample types.

2015-07-01 | E-GEOD-60447 | biostudies-arrayexpress

Time-resolved proteomic analysis of plasma membrane damage-dependent senescence

Project description:Plasma membrane damage-dependent senescence is a novel senescence subtype. Here, we compare the time-resolved proteomic profiles of plasma membrane damage-dependent senescence, DNA damage-dependent senescence, and replicative senescence to find the major differences between the senescence subtypes.

2024-12-20 | PXD047976 | JPOST Repository

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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