Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of PPARβ/δ agonist GW501516 on human and murine mesenchymal stromal cells

ABSTRACT: This study employed 3’ RNA-Seq profiling (3RSP) to investigate the transcriptomic effects of the PPARβ/δ agonist GW501516 (1 μM, 24 hours) on mesenchymal stromal cells (MSCs). Treated samples were compared with untreated controls to identify differentially expressed genes. The analysis revealed ANGPTL4 as the most significantly overexpressed gene in the treated condition across multiple experimental models, including murine and human MSCs. Importantly, this upregulation was observed in human MSCs derived from diverse tissues, such as adipose tissue, bone marrow, and umbilical cord, highlighting the consistent response of MSCs to PPARβ/δ activation across species and sources. Further functional experiments demonstrated that ANGPTL4 plays a pivotal role in enhancing the anti-apoptotic properties of MSCs. This effect was evident in both autocrine (self-regulating) and paracrine (targeting other cells) mechanisms, suggesting that ANGPTL4 may act as a key mediator of MSC-based therapeutic effect.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE283154 | GEO | 2024/11/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data of HUVEC cells after PPARβ/δ agonist and/or hypoxia treatment

2014-03-06 | GSE50378 | GEO

Expression data of HUVEC cells after PPARβ/δ agonist and/or hypoxia treatment

Project description:Recently the role of PPARβ/δ in angiogenesis has been revealed, and we hypothesized that the crosstalk between hypoxia and PPARβ/δ on endothelial cells may exsist. To elucidate the interaction between two signalings, we report the comprehensive change of transcripts induced by PPARβ/δ agonist (GW501516) and/or hypoxia. We used microarray analysis of HUVECs treated with PPARβ/δ agonist (GW501516) and/or hypoxia (1% O2) for 24-hours, and we identified a group of consistently up- or down-regulated genes. HUVECs were used within the first 6 passages. HUVECs were treated with PPARβ/δ agonist (GW501516) at a concentration of 100 nM and/or hypoxia (1% O2) for 24-hours. Same concentration of DMSO was used as a control sample, and as to the oxgen, normoxia was used as a control condition.

2014-03-06 | E-GEOD-50378 | biostudies-arrayexpress

Genome-wide maps of H3K27ac, PPARβ/δ and Pol II localization in HUVECs

Project description:H3K27Ac is one of the expressed enhancer markers, PPARβ/δ is a transcription factor and Pol II (RNA polymerase II) is an enzyme which catalyzes the transcription of DNA to synthesize precursors of mRNA and most snRNA and microRNA. These genomic localization in endothelial cells is unknown in endothelial cells. This time, we established a new antibody for H3K27ac, PPARβ/δ and Pol II and performed ChIP-seq to identify H3K27ac, PPARβ/δ and Pol II binding site in whole genome manner under PPARβ/δ agonist and/or hypoxia. We used chromatin immunoprecipitation with deep sequencing (ChIP-seq) of HUVECs treated with PPARβ/δ agonist (GW501516 100nM) and/or hypoxia (1%O2) for 24hours, then H3K27ac, PPARβ/δ and Pol II binding regions were identified. Normoxia and DMSO was used as a control condition. HUVECs were used within the first 6 passages.

2014-03-06 | E-GEOD-50144 | biostudies-arrayexpress

Effect of PPARβ/δ agonist GW501516 on human and murine mesenchymal stromal cells

Project description:Effect of PPARβ/δ agonist GW501516 on human and murine mesenchymal stromal cells

| PRJNA1192250 | ENA

ALD-PPARβ/δ

Project description:Alcoholic liver disease is a pathological condition caused by over-consumption of alcohol. Due to the high prevalence of morbidity and mortality associated with this disease, there remains a need to elucidate the molecular mechanisms underlying the etiology to develop new treatments. Since peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) modulates ethanol-induced hepatic effects, the present study examined alterations in gene expression that may contribute to this disease.

2017-01-04 | GSE86002 | GEO

Genome-wide maps of H3K27ac, PPARβ/δ and Pol II localization in HUVECs

2014-03-06 | GSE50144 | GEO

PPARβ/δ-orchestrated metabolic reprogramming supports the formation and maintenance of memory CD8+ T cells

Project description:The formation of antigen-specific memory CD8+ T cells is one of the most important features of the adaptative immune system, allowing the establishment of long-term protection against secondary infections. Although emerging evidence suggests that metabolic reprogramming is crucial for memory T cell differentiation and survival, the underlying mechanisms that drive metabolic rewiring needed for memory T cells remain unclear. Here, we found that the nuclear receptor peroxisome proliferator-activated receptor-beta/delta (PPARβ/δ) was upregulated to instruct the metabolic reprogramming, including downregulation of aerobic glycolysis and the promotion of oxidative metabolism and fatty acid oxidation, that occurs during the transition toward the establishment of central memory CD8+ T cells. Mechanistically, the exposure to interleukin-15 (IL-15) and expression of T cell factor 1 (TCF1) could coordinately activated the PPARβ/δ pathway during acute viral infection and chronic antigen exposure contexts, counteracting apoptosis induced by antigen clearance and metabolic stress. Together, our work indicates that PPARβ/δ is a master metabolic regulator orchestrating the metabolic reprogramming required for the establishment of a metabolic profile favorable for T cells longevity.

2024-08-23 | GSE264017 | GEO

PPARβ/δ-orchestrated metabolic reprogramming supports the formation and maintenance of memory CD8+ T cells [scRNA-seq]

2024-08-23 | GSE268419 | GEO

PPARβ/δ ligand response in monocyte derived macrophages

Project description:PPARβ/δ ligand response in monocyte derived macrophages

| PRJEB8757 | ENA

Identification of a novel PPARβ/δ / miR-21-3p axis in UV-induced skin inflammation [human mRNA]

Project description:Although excessive exposure to UV is widely recognized as a major factor leading to skin perturbations and cancer, the complex mechanisms underlying inflammatory skin disorders resulting from UV exposure remain incompletely characterized. The nuclear hormone receptor PPARβ/δ is known to control cutaneous repair and UV-induced cancer development. Here, we describe a novel PPARβ/δ-dependent molecular cascade involving TGFβ-1 and miR-21-3p, which is activated in the epidermis in response to UV exposure. We establish that the passenger miRNA miR-21-3p, that we identify as a novel UV-induced miRNA in the epidermis, plays a pro-inflammatory function in keratinocytes, and that its high level of expression in human skin is associated with psoriasis and squamous cell carcinomas. Finally, we provide evidence that inhibition of miR-21-3p reduces UV-induced cutaneous inflammation in ex vivo human skin biopsies, thereby underlining the clinical relevance of miRNA-based topical therapies for cutaneous disorders.

2016-06-03 | GSE80429 | GEO

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