Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

10 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Analysis of the effects of Bmx deficiency on Angiotensin II -induced cardiac hypertrophy

ABSTRACT: We show that Bmx-deficiency reduces angiotensin II -induced cardiac hypertrophy and pathological gene expression Angiotensin II or NaCl were infuced for two weeks into wild-type and Bmx-deficient mice to induce cardiac hypertrophy

ORGANISM(S): Mus musculus

SUBMITTER: Riikka Kivelä

PROVIDER: E-GEOD-47420 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Analysis of the effects of Bmx deficiency on Angiotensin II -induced cardiac hypertrophy

Project description:We show that Bmx-deficiency reduces angiotensin II -induced cardiac hypertrophy and pathological gene expression

2015-09-21 | GSE47420 | GEO

Analysis of the global gene expression in VEGF-B transgenic rat hearts

Project description:We show that an excess of VEGF-B protects the heart via adaptive cardiac hypertrophy and increased coronary arterial reserve, and by inducing a shift from lipid to glucose metabolism. Six VEGF-B overexpressing transgenic hearts were compared to six littermate wildtype controls

2013-11-30 | E-GEOD-38454 | biostudies-arrayexpress

Analysis of the global gene expression in the rat hearts transduced with adeno-associated viral vectors coding VEGF-B

Project description:We show that an excess of VEGF-B protects the heart via adaptive cardiac hypertrophy and increased coronary arterial reserve, and by inducing a shift from lipid to glucose metabolism. Six hearts transduced with AAV-VEGF-B were compared to six AAV-HSA (human serum albumin) controls

2013-11-30 | E-GEOD-38455 | biostudies-arrayexpress

PKCzeta-mediated Gaq stimulation of the ERK5 pathway is involved in cardiac hypertrophy

Project description:Background: Gq-coupled G protein-coupled receptors (GPCR) mediate the actions of a variety of messengers that are key regulators of cardiovascular function. Enhanced Gaq-mediated signaling plays an important role in cardiac hypertrophy and in the transition to heart failure. We have recently described that Gaq acts as an adaptor protein that facilitates PKCz-mediated activation of ERK5 in epithelial cells. Since the ERK5 cascade is known to be involved in cardiac hypertrophy, we have investigated the potential relevance of this pathway in Gq-dependent signaling in cardiac cells. Methodology/Principal Findings: We have explored the mechanisms involved in Gq-coupled GPCR-mediated stimulation of the ERK5 pathway and its functional consequences in cardiac hypertrophy using both cultured cardiac cells and an animal model of angiotensin- dependent induction of cardiac hypertrophy in wild-type and PKCz knockout mice. We find that PKC? is required for the activation of the ERK5 pathway by Gq-coupled GPCR in cardiomyocytes and in cardiac fibroblasts. Stimulation of ERK5 by angiotensin II is blocked upon pharmacological inhibition or siRNA-mediated silencing of PKCz in primary cultures of cardiac cells and in cardiomyocytes isolated from PKCz-deficient mice. Moreover, these mice do not develop cardiac hypertrophy upon chronic challenge with angiotensin II, as assessed by morphological, biomarker, electrocardiographic and global gene expression pattern analysis. Conclusion/Significance: Our data put forward that PKC? is essential for Gq- dependent ERK5 activation in cardiac cells and indicate a key cardiac physiological role for this recently described Gaq/PKCz/MEK5 signaling axis. Littermate wild-type and PKCz -/- male mice (32 weeks of age) were subjected to continuous infusion of angiotensin II (or PBS as a control) for 14 days, a well established model for the induction of cardiac hypertrohy

2012-01-10 | E-GEOD-29145 | biostudies-arrayexpress

Cardiac hypertrophy and failure

Project description:Analysis of cardiac specific AT1 transgenic mice undergoing cardiac failure, cardiac hypertrophy and wild type aged matched controls. For detailed description of the AT1 Tg mice please refer to: Paradis P, Dali-Youcef N, Paradis FW, Thibault G, Nemer M. Overexpression of angiotensin II type I receptor in cardiomyocytes induces cardiac hypertrophy and remodeling. Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):931-6. PMID: 10639182 [PubMed - indexed for MEDLINE] Keywords: ordered

2005-06-15 | GSE2355 | GEO

Transcription profiling of mouse AT1 transgenics undergoing cardiac failure, cardiac hypertrophy and wild type aged matched controls

Project description:Analysis of cardiac specific AT1 transgenic mice undergoing cardiac failure, cardiac hypertrophy and wild type aged matched controls. For detailed description of the AT1 Tg mice please refer to:; Paradis P, Dali-Youcef N, Paradis FW, Thibault G, Nemer M. Overexpression of angiotensin II type I receptor in cardiomyocytes induces cardiac hypertrophy and remodeling. Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):931-6. PMID: 10639182 [PubMed - indexed for MEDLINE]

2008-06-12 | E-GEOD-2355 | biostudies-arrayexpress

RORa regulates developmental and angiotensin II-induced cardiac hypertrophy

Project description:RORasg/sg mice have small cardiomyocytes and hypocontractile hearts with increased fibrosis. Microarrays revealed broad deficits of sarcomeric RNAs and key myogenic transcription factors, suggesting that the loss of RORa leads to impaired developmental hypertrophy through transcriptional regulation. RORasg/sg mice developed exaggerated ventricular remodeling in response to Agn II infusion. We identify novel cardioprotective roles for RORa in promoting developmental and preventing pathological cardiac hypertrophy, mediated in part through regulation of the IL-6-STAT3 pathway in cardiomyocytes and cardiac fibrosis

2021-04-12 | GSE98892 | GEO

Expression data of murine model of cardiac hypertrophy

Project description:An initial cellular change in the pathogenesis of heart failure is cardiomyocyte hypertrophy, characterized by increased cell size, enhanced protein synthesis and reactivation of fetal genes. In addition to mechanical stresses, several neurohumoral factors have been identified as potent hypertrophic agents, including angiotensin II, endothelin, and catecholamines. We used microarrays to study the gene expression during cardiac hypertrophy.

2011-12-31 | GSE26671 | GEO

PKCz-mediated Gaq stimulation of the ERK5 pathway is involved in cardiac hypertrophy

Project description:Background: Gq-coupled G protein-coupled receptors (GPCR) mediate the actions of a variety of messengers that are key regulators of cardiovascular function. Enhanced Gaq-mediated signaling plays an important role in cardiac hypertrophy and in the transition to heart failure. We have recently described that Gaq acts as an adaptor protein that facilitates PKCz-mediated activation of ERK5 in epithelial cells. Since the ERK5 cascade is known to be involved in cardiac hypertrophy, we have investigated the potential relevance of this pathway in Gq-dependent signaling in cardiac cells. Methodology/Principal Findings: We have explored the mechanisms involved in Gq-coupled GPCR-mediated stimulation of the ERK5 pathway and its functional consequences in cardiac hypertrophy using both cultured cardiac cells and an animal model of angiotensin- dependent induction of cardiac hypertrophy in wild-type and PKCz knockout mice. We find that PKCζ is required for the activation of the ERK5 pathway by Gq-coupled GPCR in cardiomyocytes and in cardiac fibroblasts. Stimulation of ERK5 by angiotensin II is blocked upon pharmacological inhibition or siRNA-mediated silencing of PKCz in primary cultures of cardiac cells and in cardiomyocytes isolated from PKCz-deficient mice. Moreover, these mice do not develop cardiac hypertrophy upon chronic challenge with angiotensin II, as assessed by morphological, biomarker, electrocardiographic and global gene expression pattern analysis. Conclusion/Significance: Our data put forward that PKCζ is essential for Gq- dependent ERK5 activation in cardiac cells and indicate a key cardiac physiological role for this recently described Gaq/PKCz/MEK5 signaling axis.

2012-01-10 | GSE29145 | GEO

Rat models of cardiac hypertrophy

Project description:Cardiac hypertrophy was induced by aortic banding (6, 12, 16, and 30 weeks), myocardial infarction (3 and 9 weeks), an av-fistula (aorta abd. to v. cava inf.. 3 and 8 weeks), or hormone infusion (two weeks either angiotensin 2 or a thyroxin analogue). Sham operated or saline infused animals served as controls. Gene expression was determined by Affymetrix RGU34A GeneChip's to identify genes with common regulation in the different models of cardiac hypertrophy. Keywords: other

2004-03-12 | GSE738 | 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