Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PPAR-gamma-activating Angiotensin Type 1 Receptor Blockers

ABSTRACT: expression pattern of adipocytes after telmisartan, pioglitazone or irbesartan treatment Keywords: repeat sample

ORGANISM(S): Mus musculus

PROVIDER: GSE2486 | GEO | 2005/04/05

SECONDARY ACCESSION(S): PRJNA91883

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of mouse adipocytes after telmisartan, pioglitazone or irbesartan treatment

Project description:expression pattern of adipocytes after telmisartan, pioglitazone or irbesartan treatment

2008-06-12 | E-GEOD-2486 | biostudies-arrayexpress

Connectivity mapping of angiotensin-PPAR interactions involved in the amelioration of non-alcoholic steatohepatitis by Telmisartan

Project description:Nonalcoholic fatty liver disease (NAFLD) is a rapidly increasing global health problem that is associated with metabolic disorders covering a broad spectrum of pathological abnormalities, including simple steatosis, nonalcoholic steatohepatitis (NASH), advanced fibrosis and cirrhosis, and hepatocellular carcinoma (HCC). Telmisartan is a potential treatment for NAFLD due to its ability to improve insulin sensitivity and decrease hepatic fat accumulation via modulation of peroxisome proliferator-activated receptor gamma (PPARγ), and to suppress hepatic fibrosis by blocking angiotensin II receptors. However, the underlying molecular mechanisms of action of telmisartan, and the interaction between the renin-angiotensin system (RAS) and PPAR, have yet to be fully elucidated. Thus, in the present study, NASH-HCC STAM mice received daily administrations of telmisartan for 6 weeks to assess the prevention of fibrosis and lipid accumulation in the liver, and to evaluate improvements in NASH. Hepatic transcriptome analyses revealed that the amelioration of NASH likely occurred through the regulation of inflammatory- and fibrosis-related gene responses. An integrated protein-protein interaction network analysis including transcriptional and non-transcriptional genes regulated by telmisartan showed that the NAFLD pathway is located at the center of the network and has interconnections with the RAS and PPAR signaling pathways. Additionally, the downstream targets of the transcription factors in the network, PPARα, PPARδ, and RELA, significantly overlapped with telmisartan-induced differentially expressed genes (DEGs). This alternative approach to assessing the transcriptome provided the opportunity to understand the fundamental molecular mechanisms underpinning the therapeutic effects of telmisartan, and will contribute to the establishment of a novel pharmacological treatment for NASH patients.

2019-03-19 | GSE120937 | GEO

Transcriptomic profile of porcine corpus luteum after PPAR gamma ligands treatment

Project description:The corpus luteum plays a critical role in reproduction because it is the primary source of circulating progesterone. This study aimed to determine the in vitro effect of peroxisome proliferator-activated receptor gamma (PPARγ) ligands on the transcriptome genes expression in the porcine corpus luteum in the mid- and late-luteal phase of the estrous cycle using RNA-seq technology. The corpus luteum slices were incubated in vitro in the presence of PPARγ agonist – pioglitazone and antagonist—T0070907. We identified 40 differentially expressed genes after pioglitazone treatment and 40 after T0070907 treatment in the mid-luteal phase as well as 26 after pioglitazone and 29 after T0070907 treatment in late-luteal phase of the estrous cycle. In addition, we detected differences in genes expression between the mid- and late-luteal phase without treatment (409). These results should become a basis for further studies explaining the mechanism of PPARγ action in the reproductive system in pigs.

2022-11-15 | E-MTAB-11964 | biostudies-arrayexpress

Common angiotensin receptor blockers may directly modulate the immune system via VDR, PPAR and CCR2b.

Project description: Not available

| S-EPMC1360063 | biostudies-literature

Apoptosis rate and transcriptional response of pancreatic islets exposed to the PPAR gamma agonist Pioglitazone

2012-08-16 | GSE40119 | GEO

Apoptosis rate and transcriptional response of pancreatic islets exposed to the PPAR gamma agonist Pioglitazone

Project description:To explore the molecular pathways underlying thiazolidinediones effects on pancreatic islets in conditions mimicking normo- and hyperglycemia, apoptosis rate and transcriptional response to Pioglitazone at both physiological and supraphysiological glucose concentrations were evaluated. Adult rat islets were cultured at physiological (5.6 mM) and supraphysiological (23 mM) glucose concentrations in presence of 10 mM Pioglitazone or vehicle. RNA expression profiling was evaluated with the PancChip 13k cDNA microarray after 24-h, and expression results for some selected genes were validated by qRT-PCR.

2012-08-16 | E-GEOD-40119 | biostudies-arrayexpress

Angiotensin receptor blockers and COVID-19.

Project description: Not available

| S-EPMC7158830 | biostudies-literature

Synthetic nanobodies as angiotensin receptor blockers.

Project description: Not available

| S-EPMC7443875 | biostudies-literature

Association Between Angiotensin-Converting Enzyme Inhibitors, Angiotensin Receptor Blockers, and Suicide.

Project description: Not available

| S-EPMC6806420 | biostudies-literature

Comparative Transcriptional Network Modeling of Three PPAR-α/γ Co-agonists Reveals Distinct Metabolic Gene Signatures in Primary Human Hepatocytes

Project description:Aims: To compare the molecular and biologic signatures of a balanced dual peroxisome proliferator-activated receptor-α/γ (PPAR-α/γ) agonist, aleglitazar, with tesaglitazar (a dual PPAR-α/γ agonist) or combination of pioglitazone (PPAR-γ agonist)/fenofibric acid (PPAR-α agonist) in human hepatocytes. Methods and Results: Gene expression microarray profiles were obtained from primary human hepatocytes treated with EC50-aligned low, medium, and high concentrations of the three treatments. A systems-biology approach, Causal Network Modeling, was used to model the data to infer upstream molecular mechanisms that may explain the observed changes in gene expression. Aleglitazar, tesaglitazar and pioglitazone/fenofibric acid, each induced unique transcriptional signatures, despite comparable core PPAR signaling. Although all treatments inferred qualitatively similar PPAR-α signaling, aleglitazar was inferred to have greater effects on high- and low-density lipoprotein cholesterol levels than tesaglitazar and pioglitazone/fenofibric acid, due to greater number of gene expression changes in pathways related to HDL and LDL metabolism. Distinct transcriptional and biologic signatures were also inferred for stress responses, which appeared to be less affected by aleglitazar than the comparators. In particular, pioglitazone/fenofibric acid was inferred to increase NFE2L2 activity, a key component of the stress response pathway, while aleglitazar had no significant effect. All treatments were inferred to decrease proliferative signaling. Conclusions: Aleglitazar induces transcriptional signatures related to lipid parameters and stress responses that are unique from other dual PPAR-α/γ treatments. This may underlie observed favorable changes in lipid profiles in animal and clinical studies with aleglitazar and suggests a differentiated gene profile compared with other dual PPAR-α/γ agonist treatments.

2011-10-22 | GSE33152 | GEO

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