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ChIP assay in adult ventricular cardiomyocytes

ABSTRACT: ChIP assay was performed to study the genomic location of SRF myocytes cistrome in adult ventricular cardiomyocytes. The myocytes were stimulated by phenylephrine (PE) combined with adenoviral overexpression of SRF serine-103 mutants.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE134799 | GEO | 2020/12/09

REPOSITORIES: GEO

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PRO-seq assay in adult ventricular cardiomyocytes

Project description:PRO-seq assay was performed for the quantitative detection of nascent pre-mRNA transcripts induced by phenylephrine (PE) and adenoviral overexpression of SRF serine-103 mutants in adult ventricular cardiomyocytes

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Transcription profiling of rat neonatal ventricular cardiomyocytes (NRVCMs) stretched biaxially (112%/24h) or stimulated with phenylephrine (PE, 50 uM

Project description:Neonatal rat ventricular cardiomyocytes (NRVCMs) were stretched biaxially (112%/24h) or stimulated with phenylephrine (PE, 50 uM), both resulting in a similar degree of hypertrophy. Unstretched NRVCMs served as negative control. Affymetrix microarray analysis revealed 164 genes more than 2.0-fold up- and 21 genes less than 0.5-fold downregulated (p<0.01). Differential expression was confirmed by real-time PCR. Several genes of the âfetal gene programâ, i.e. BNP (4.2-fold, all p<0.05) were induced by stretch as well as PE. We also verified the upregulation of known stretch-responsive genes, including HSP70 (20.9x) and c-myc (3.0x). Moreover, we identified genes exclusively induced by stretch, such as the cardioprotective and antihypertrophic cytokine GDF15 (24.8x) and the antihypertrophic factor heme oxygenase 1 (Hmox1, 10.8x; both confirmed on protein level). Of note, neither PE nor endothelin-1 were able to upregulate GDF15 and Hmox1, while angiotensin II significantly induced both genes. Conversely, addition of the AT1 receptor blocker irbesartan markedly blunted stretch-mediated GDF15 and Hmox1 induction, suggesting that the angiotensin II receptor mediates stretch-dependent signals. In conclusion, we report a comprehensive gene expression profile of cardiomyocytes subjected to biomechanical stress in comparison to pharmacologically induced hypertrophy. Our data imply that a stretch-specific gene program exists, that is mediated, at least in part, by angiotensin-II-dependent signalling. Experiment Overall Design: Three conditions were compared with two replicates each. These are: Experiment Overall Design: (1) control, i.e. no treatment; (2) induction by phenylephrine (50 uM); (3) induction by biomechanical stretch (112%/24h)

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