Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

8 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of young and senescent human umbilical vein endothelial cells (HUVECs) under normal or high glucose conditions

ABSTRACT: Human endothelial cellular models are useful to disentangle the pathophysiological role of dysfunctional endothelium in the development of cardiovascular (CV) disease and organ damage in T2D. Here, we performed a RNAseq of human umbilical vein endothelial cells (HUVECs) undergoing replicative senescence and exposed to high glucose (25 mM) to investigate the combined effects of replicative senescence and high glucose on the transcriptional landscape of these cells. To gain insight into the molecular mechanisms driving the acquisition of a senescent phenotype following exposure to HG, we performed a RNA-seq assay on control (Ctr) and replicative senescent (Sen) HUVECs cultivated in presence/absence of HG culture medium (total number of samples = 12; number of samples in each cell type-medium condition group = 3) using the NovaSeq 6000 Illumina system. Differential expression analysis was performed in R environment (version 4.2.2) using the limma and edgeR Bioconductor R packages.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Homo sapiens

SUBMITTER: Jacopo Sabbatinelli

PROVIDER: E-MTAB-13959 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Myeloma cancer cells can corrupt mesenchymal stromal senescent cells and impair their anti-tumor activity

Project description:Senescent cells secrete many molecules, which contribute to the prevention of cancer progression. We induced MSC senescence by oxidative stress, DNA damage, and replicative exhaustion. The first two are considered inducers of acute senescence while extensive proliferation triggers replicative senescence also named chronic senescence. We cultivated cancer cells in the presence of acute and chronic senescent MSC conditioned media and evaluated proliferation, DNA damage, apoptosis and senescence.

2018-10-25 | PXD003018 | Pride

MicroRNA profiling of human umbical vein endothelial cells (HUVEC) using young (replicating) cells and senescent cells

Project description:From two donors of human umbilical vein endothelial cells, in vitro cell lines were established. Both cell lines were grown in vitro until irreversible growth arrest was observed (replicative senescence). Total RNA from young (replicating) cells as well as senescent cells was harvested and used for hybridization of microRNA chips (MRC) from TU Graz based on Sanger miRBase 9.2

2010-04-19 | E-MEXP-2425 | biostudies-arrayexpress

Replicative senescence is associated with nuclear reorganization and DNA methylation at specific transcription factor binding sites (RNA-seq)

Project description:Primary cells enter replicative senescence after a limited number of cell divisions. This process is associated with reproducible changes in DNA methylation (DNAm) at specific sites in the genome. The mechanism that drives senescence-associated DNAm changes remains unknown and may arise through drift in DNAm or through regulated, senescence dependent modifications at specific sites in the genome. In this study, we analyzed the reorganization of nuclear architecture and DNA methylation during long-term culture of human fibroblasts and mesenchymal stromal cells (MSCs). [RNA-seq] RNA was isolated from 1,000,000 cells of three MSC donors (59, 64, and 73 years old) at passage 4 and passage 13 using the miRNeasy Mini Kit (Qiagen). Gene expression profiles were analzyed by deep sequencing with IlluminaHiSeq 2000 technology with a read length of 50 bases at EMBL gene core facility (Heidelberg, Germany).

2015-03-26 | E-GEOD-59966 | biostudies-arrayexpress

Real-time quantitative PCR analysis of Human Umbilical Vein Endothelial Cells (HUVEC)

Project description:In order to identify new markers of vascular cell senescence with potential in vivo implications, primary cultured Human Umbilical Vein Endothelial Cells (HUVECs), were analysed for microRNA (miR) expression. QRT-PCR microRNA expression profiling in 3 senescent (XIII passage) vs. 3 young HUVECs (II passage).

2012-05-15 | E-GEOD-37972 | biostudies-arrayexpress

Replicative senescence is associated with nuclear reorganization and DNA methylation at specific transcription factor binding sites (MBD-seq)

Project description:Primary cells enter replicative senescence after a limited number of cell divisions. This process is associated with reproducible changes in DNA methylation (DNAm) at specific sites in the genome. The mechanism that drives senescence-associated DNAm changes remains unknown and may arise through drift in DNAm or through regulated, senescence dependent modifications at specific sites in the genome. In this study, we analyzed the reorganization of nuclear architecture and DNA methylation during long-term culture of human fibroblasts and mesenchymal stromal cells (MSCs). [MethylCap-seq] Fibroblasts of two female donors (both 43 years old) were culture expanded and DNA was harvested of 10,000,000 cells at early passage (P3 or P5) and late passage (P30 and P33). DNA methylation changes were subsequently analyzed by MethylCap-Seq.

2015-03-26 | E-GEOD-59960 | biostudies-arrayexpress

A miR-494 dependent feedback loop regulates ER stress (ANAN-376 Project)

Project description:Defects in stress responses are important contributors in many chronic conditions including cancer, cardiovascular disease, diabetes, and obesity-driven pathologies like non-alcoholic steatohepatitis (NASH). Specifically, endoplasmic reticulum (ER) stress is linked with these pathologies and control of ER stress can ameliorate tissue damage. MicroRNAs have a critical role in regulating diverse stress responses including ER stress. Here we show that miR-494-3p plays a functional role during ER stress. ER stress inducers (tunicamycin and thapsigargin) robustly increase the expression of miR-494 in vitro in an ATF6 dependent manner. Surprisingly, miR-494 pretreatment dampens the induction and magnitude of ER stress in response to tunicamycin in endothelial cells. Conversely, inhibition of miR-494 increases ER stress de novo and amplifies the effects of ER stress inducers. Using Mass Spectrometry (TMT-MS) we identified many proteins that are downregulated by both tunicamycin and miR-494 in cultured human umbilical vein endothelial cells (HUVECs). Among these, we found 6 transcripts which harbor a putative miR-494 binding site. Our data indicates that ER stress driven miR-494 may act in a feedback inhibitory loop to dampen downstream ER stress signaling. We propose that RNA-based approaches targeting miR-494 or its targets may be attractive candidates for inhibiting ER stress dependent pathologies in human disease.

2021-09-09 | PXD019992 | Pride

Senescence-associated lncRNAs: senescence-associated long noncoding RNAs.

Project description:Noncoding RNAs include small transcripts, such as microRNAs and piwi-interacting RNAs, and a wide range of long noncoding RNAs (lncRNAs). Although many lncRNAs have been identified, only a small number of lncRNAs have been characterized functionally. Here, we sought to identify lncRNAs differentially expressed during replicative senescence. We compared lncRNAs expressed in proliferating, early-passage, 'young' human diploid WI-38 fibroblasts [population doubling (PDL) 20] with those expressed in senescent, late-passage, 'old' fibroblasts (PDL 52) by RNA sequencing (RNA-Seq). Numerous transcripts in all lncRNA groups (antisense lncRNAs, pseudogene-encoded lncRNAs, previously described lncRNAs and novel lncRNAs) were validated using reverse transcription (RT) and real-time, quantitative (q)PCR. Among the novel senescence-associated lncRNAs (SAL-RNAs) showing lower abundance in senescent cells, SAL-RNA1 (XLOC_023166) was found to delay senescence, because reducing SAL-RNA1 levels enhanced the appearance of phenotypic traits of senescence, including an enlarged morphology, positive Î²-galactosidase activity, and heightened p53 levels. Our results reveal that the expression of known and novel lncRNAs changes with senescence and suggests that SAL-RNAs play direct regulatory roles in this important cellular process. RNA was extracted from both young and senescent WI-38 cells and used for total RNA-Seq.

2016-02-08 | E-GEOD-77675 | biostudies-arrayexpress

Replicative senescence is associated with nuclear reorganization and DNA methylation at specific transcription factor binding sites

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-03-26 | E-GEOD-59979 | biostudies-arrayexpress

H3K9me3 ChIPseq experiments from PD IMR90s

Project description:H3K9me3 ChIPseq in Proliferating and Senescent IMR90s We used ChIP-seq to examine the global binding of H3K9me3 in human IMR90 replicative senescence (RS) and oncogene-induced (OIS)

2014-12-15 | E-GEOD-53329 | biostudies-arrayexpress

WGS for B16-OVA and 4T1 murine cancer cell lines

Project description:Whole Genome Sequencing of the murine breast cancer cell line 4T1 and of the murine melanoma cell line B16-ova was carried out with the aim of identifying somatic mutations. We also ran deep Mass Spectrometry proteomics analysis on the same cell lines, aiming to determine which somatic mutations carry over to the protein expression level. Further, we tested these cancer specific protein epitopes (putative neoantigens) for immunogenicity using mouse models. Finally, the putative neoantigens that showed good immunogenic potential were used in tumor growth control experiments with mice engrafted with the two tumor cell lines. In these experiments we tested whether cancer vaccines based on individual neoantigen peptides (MHC-I) restricted the growth of the tumor compared to adequate controls. The overall aim of the project is to validate the ability of our multi-omics/bioinformatics pipeline to identify and deliver neoantigens that can be used to suppress tumor growth. File names Sample names P10859_101_S1_L001_R1_001_BHKWV3CCXY 4T1_S1_L001_R1_001_BHKWV3CCXY P10859_101_S1_L001_R2_001_BHKWV3CCXY 4T1_S1_L001_R2_001_BHKWV3CCXY P10859_101_S1_L002_R1_001_BHKWV3CCXY 4T1_S1_L002_R1_001_BHKWV3CCXY P10859_101_S1_L002_R2_001_BHKWV3CCXY 4T1_S1_L002_R2_001_BHKWV3CCXY P10859_102_S2_L003_R1_001_BHKWV3CCXY B16-OVA_S2_L003_R1_001_BHKWV3CCXY P10859_102_S2_L003_R2_001_BHKWV3CCXY B16-OVA_S2_L003_R2_001_BHKWV3CCXY P10859_102_S2_L004_R1_001_BHKWV3CCXY B16-OVA_S2_L004_R1_001_BHKWV3CCXY P10859_102_S2_L004_R2_001_BHKWV3CCXY B16-OVA_S2_L004_R2_001_BHKWV3CCXY

2024-01-31 | E-MTAB-13635 | biostudies-arrayexpress

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