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Expression data from adult (9 month-old) and young (4 month-old) hearts from GRK2 heterozygous C57BL/6J mice.

ABSTRACT: G protein-coupled receptor kinase 2 (GRK2) has emerged as a key regulator of cardiac function and myocardial structure. Cardiac GRK2 is increased in heart failure and ischemia in humans, whereas genetic inhibition of GRK2 is cardioprotective in animal models of these pathologies. However, the mechanistic basis underlying these effects are not fully understood. We have used adult GRK2 hemizygous mice (GRK2+/-) as a model to assess the effects of a sustained systemic inhibition of GRK2 in heart tissue with age. We used microarrays to determine the global programme of gene expression underlying cardioprotection in GRK2 hemizygous mice with age.

ORGANISM(S): Mus musculus

PROVIDER: GSE41808 | GEO | 2012/10/25

SECONDARY ACCESSION(S): PRJNA178239

REPOSITORIES: GEO

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Expression data from adult (9 month-old) and young (4 month-old) hearts from GRK2 heterozygous C57BL/6J mice.

Project description:G protein-coupled receptor kinase 2 (GRK2) has emerged as a key regulator of cardiac function and myocardial structure. Cardiac GRK2 is increased in heart failure and ischemia in humans, whereas genetic inhibition of GRK2 is cardioprotective in animal models of these pathologies. However, the mechanistic basis underlying these effects are not fully understood. We have used adult GRK2 hemizygous mice (GRK2+/-) as a model to assess the effects of a sustained systemic inhibition of GRK2 in heart tissue with age. We used microarrays to determine the global programme of gene expression underlying cardioprotection in GRK2 hemizygous mice with age. 9 month-old and 4 month-old mice hearts were collected for RNA extraction and hybridization on Affymetrix microarrays.

2012-10-25 | E-GEOD-41808 | biostudies-arrayexpress

Expression data from young (4 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates

2012-10-25 | GSE41809 | GEO

Expression data from adult (9 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates

2012-10-20 | GSE41706 | GEO

Expression data from adult (9 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates

Project description:G protein-coupled receptor kinase 2 (GRK2) has emerged as a key regulator of cardiac function and myocardial structure. Cardiac GRK2 is increased in heart failure and ischemia in humans, whereas genetic inhibition of GRK2 is cardioprotective in animal models of these pathologies. However, the mechanistic basis underlying these effects are not fully understood. We have used adult GRK2 hemizygous mice (GRK2+/-) as a model to assess the effects of a sustained systemic inhibition of GRK2 in heart tissue with age. We used microarrays to determine the global programme of gene expression underlying cardioprotection in GRK2 hemizygous mice. 9 month-old mice hearts were collected for RNA extraction and hybridization on Affymetrix microarrays.

2012-10-20 | E-GEOD-41706 | biostudies-arrayexpress

Expression data from young (4 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates

Project description:G protein-coupled receptor kinase 2 (GRK2) has emerged as a key regulator of cardiac function and myocardial structure. Cardiac GRK2 is increased in heart failure and ischemia in humans, whereas genetic inhibition of GRK2 is cardioprotective in animal models of these pathologies. However, the mechanistic basis underlying these effects are not fully understood. We have used adult GRK2 hemizygous mice (GRK2+/-) as a model to assess the effects of a sustained systemic inhibition of GRK2 in heart tissue with age. We used microarrays to determine the global programme of gene expression underlying cardioprotection in GRK2 hemizygous mice. 4 month-old mice hearts were collected for RNA extraction and hybridization on Affymetrix microarrays.

2012-10-25 | E-GEOD-41809 | biostudies-arrayexpress

Expression data from adult (9 month-old) and young (4 month-old) hearts from C57BL/6J mice

Project description:G protein-coupled receptor kinase 2 (GRK2) has emerged as a key regulator of cardiac function and myocardial structure. Cardiac GRK2 is increased in heart failure and ischemia in humans, whereas genetic inhibition of GRK2 is cardioprotective in animal models of these pathologies. However, the mechanistic basis underlying these effects are not fully understood. We have used adult GRK2 hemizygous mice (GRK2+/-) as a model to assess the effects of a sustained systemic inhibition of GRK2 in heart tissue with age. We used microarrays to determine the global programme of gene expression underlying cardioprotection with age in GRK2 hemizygous mice in comparation with their wild-type littermates.

2012-10-25 | GSE41807 | GEO

Expression data from adult (9 month-old) and young (4 month-old) hearts from C57BL/6J mice

Project description:G protein-coupled receptor kinase 2 (GRK2) has emerged as a key regulator of cardiac function and myocardial structure. Cardiac GRK2 is increased in heart failure and ischemia in humans, whereas genetic inhibition of GRK2 is cardioprotective in animal models of these pathologies. However, the mechanistic basis underlying these effects are not fully understood. We have used adult GRK2 hemizygous mice (GRK2+/-) as a model to assess the effects of a sustained systemic inhibition of GRK2 in heart tissue with age. We used microarrays to determine the global programme of gene expression underlying cardioprotection with age in GRK2 hemizygous mice in comparation with their wild-type littermates. 9 month-old and 4 month-old mice hearts were collected for RNA extraction and hybridization on Affymetrix microarrays.

2012-10-25 | E-GEOD-41807 | biostudies-arrayexpress

Cardiac transcriptome analysis of RKIP-transgenic and GRK2-transgenic mice by NGS

Project description:The RAF kinase inhibitor protein, RKIP, is a dual inhibitor of the RAF1 kinase and the G-protein-coupled receptor kinase 2 (GRK2). By inhibition of the proto-oncogenic and pro-survival RAF1-MAPK pathway, the RAF kinase inhibitor protein, RKIP, acts as a tumor suppressor, which enhances cardiomyocyte death and promotes the development of symptoms of heart failure. To elucidate pathomechanisms of heart failure induced by RKIP, the study determined the cardiac transcriptomes of eight-month-old, male, transgenic mice with cardiac-specific expression of RKIP (PEBP1) under control of the myocardium-specific, alpha-MHC promoter. In addition, the study determined the cardiac transcriptomes of GRK2-transgenic mice. Tg-GRK2 mice have a slightly increased transgenic expression of GRK2. According to NGS data, cardiac GRK2-Grk2 transcript levels of Tg-GRK2 mice are 1.59±0.10-fold higher than those of non-transgenic FVB hearts. In Tg-GRK2 mice, transgenic GRK2 is expressed under control of the ubiquitous CMV immediate-early promoter/enhancer. The non-transgenic control group are age-matched, male, nontransgenic FVB/N mice. NGS data of this study document transcriptome changes underlying the heart failure phenotype induced by transgenic RKIP expression and cardiac degeneration induced by GRK2 expression.

2021-12-27 | GSE191316 | GEO

Whole genome cardiac gene expression profiling of transgenic mice with myocardium-specific expression of RKIP (PEBP1), kinase-inactive GRK2-K220R (ADRBK1-K220R), SCD1, and UCP1

Project description:The raf kinase inhibitor protein, RKIP, is up-regulated on cadiac biopsy specimens of heart failure patients. To investigate the in vivo role of an increased cardiac content of RKIP, we generated transgenic mice with myocardium-specific expression of RKIP (PEBP1; phosphatidylethanolamine binding protein 1) under control of the alpha-MHC promoter in B6 (C57BL/6J) background. Because RKIP is a dual-specific GRK2 and Raf kinase inhibitor, RKIP-transgenic mice were compared to transgenic mice with myocardium-specific expression of the GRK2 inhibitor, GRK2-K220R, which is a kinase-inactive GRK2 (ADRBK1) mutant with dominant-negative function. In frame of our studies, we found that RKIP-transgenic mice developed signs of heart failure and cardiotoxic lipid load at an age of 8 months. In contrast, transgenic expression of GRK2-K220R improved cardiac function and protected against chronic pressure overload-induced symptoms of heart failure. To identify genes related to cardiotoxic lipid load, we further determined the cardiac gene expression profile of Tg-SCD1 mice with mypcardium-specific expression of SCD1 (stearoyl-CoA desaturase-1) and Tg-UCP1 mice with heart-specific expression of UCP1 (uncoupling protein 1).

2018-09-18 | GSE120020 | GEO

Microarray gene expression profiling of transgenic mice with myocardium-specific expression of RKIP or a GRK-specific peptide inhibitor

Project description:The Raf kinase inhibitor protein (RKIP) is a dual inhibitor of the Raf kinase and the G-protein-coupled receptor kinase 2 (GRK2). GRK2 is an indispensable kinase, which exerts a major role in the pathogenesis of heart failure, and inhibition of GRK2 is cardioprotective in experimental models of heart failure. To investigate the cardiac function of RKIP as GRK2 inhibitor, we generated transgenic mice with myocardium-specific expression of RKIP under control of the alpha-MHC promoter. For comparison, mice with myocardium-specific expression of a GRK-specific peptide inhibitor (GRK-Inh) were also generated. Two different transgenic mouse models were established. Transgenic RKIP mice and transgenic GRK-Inh mice were born at Mendelian frequencey and grew to adulthood normally. Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) RKIP-transgenic mice, (ii) GRK-Inh-transgenic mice, and (iii) B6 control mice.

2012-12-06 | E-GEOD-42753 | biostudies-arrayexpress

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