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The translational landscape of phenylephrine-treated neonatal rat cardiomyocytes [nsRNA-seq]

ABSTRACT: The translational landscape of phenylephrine-treated neonatal rat cardiomyocytes [nsRNA-seq]

PROVIDER: PRJNA713922 | ENA |

REPOSITORIES: ENA

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The translational landscape of phenylephrine-treated neonatal rat cardiomyocytes

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A Comparison of Neonatal Rat Ventricular Myocytes Treated With Phenylephrine or PAMH

Project description:Neonatal rat ventricular myocytes cultured for 48 hours without stimulation, in the presence of twenty micromolar phenylephrine, or in the presence of one micromolar PAMH. Keywords = Rattus Keywords = Ventricular Myocytes Keywords = Cardiomyocytes Keywords = Hypertrophy Keywords = Phenylephrine Keywords = PAMH Keywords = 5-hydroxytryptamine Keywords = Pyridine Keywords: repeat sample

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The translational landscape of phenylephrine-treated neonatal rat cardiomyocytes [ssRNA-seq]

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2021-03-11 | GSE155913 | GEO

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Transcription profiling by array of Rattus norvegicus cardiomyocytes to investigate the effects of 30 or 60 min phenylephrine exposure on gene expression

Project description:Rat neonatal cardiomyocytes were exposed to 100 uM phenylephrine for 0, 30 or 60 mins

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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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The translational landscape of phenylephrine-treated neonatal rat cardiomyocytes

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-03-11 | GSE155914 | GEO