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PRO-seq assay in adult ventricular cardiomyocytes

ABSTRACT: 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

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE134800 | GEO | 2020/12/09

REPOSITORIES: GEO

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ChIP assay in adult ventricular cardiomyocytes

Project description: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.

2020-12-09 | GSE134799 | GEO

PRO-seq assay in adult ventricular cardiomyocytes

Project description:PRO-seq assay 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)

2008-06-14 | E-GEOD-5996 | biostudies-arrayexpress

ChIP assay in adult ventricular cardiomyocytes

Project description:ChIP assay in adult ventricular 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

2004-03-02 | GSE925 | GEO

LncRNA Chaer contributes to the transcriptome reprogramming during phenylephrine-induced hypertrophy in neonatal rat ventricular myocytes

Project description:We compared the transcriptome modified by siRNA-mediated cardiac hypertrophy associated epigenentic regulator (Chaer) with negative control siRNA treated neonatal rat ventricular myocytes with or without phenylephrine treatment. The results suggest that Chaer knockdown broadly blocks the phenylephrine-induced hypertrophic programming of the transcriptome. Transcripts profiles from neonatal rat ventricular myocytes with or without phenylephrine and with or without Chaer-specific siRNA compared to negative control siRNA

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Adult ventricular cardiomyocytes

Project description:Adult ventricular cardiomyocytes

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Transcription profiling 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.

2008-06-16 | E-GEOD-925 | biostudies-arrayexpress

LncRNA Chaer contributes to the transcriptome reprogramming during phenylephrine-induced hypertrophy in neonatal rat ventricular myocytes

2016-06-30 | GSE82339 | GEO

Hypertrophy induced KIF5B controls mitochondrial localization and function in neonatal rat cardiomyocytes

Project description:Cardiac hypertrophy is associated with growth and functional changes of cardiomyocytes,including mitochondrial alterations, but the latter are still poorly understood. Here we investigated mitochondrial function and dynamic localization in neonatal rat ventricular cardiomyocytes (NRVCs) stimulated with insulin like growth factor 1 (IGF1) or phenylephrine (PE), mimicking physiological and pathological hypertrophic responses,respectively. A decreased activity of the mitochondrial electron transport chain (ETC) (state 3) was observed in permeabilized NRVCs stimulated with PE, whereas this was improved in IGF1 stimulated NRVCs. In contrast, in intact NRVCs, mitochondrial oxygen consumption rate (OCR) was increased in PE stimulated NRVCs, but remained constant in IGF1 stimulated NRVCs. After stimulation with PE, mitochondria localized to the periphery of the cell. To study the differences in more detail, we performed gene array studies. IGF1 and PE stimulated NRVCs did not reveal major differences in gene expression of mitochondrial encoding proteins, but we identified a gene encoding amotor protein implicated in mitochondrial localization, kinesin family member 5b (Kif5b ), which was clearly elevated in PE stimulated NRVCs but not in IGF1 stimulated NRVCs. We confirmed that Kif5b gene and protein expression was elevated in animal models with pathological cardiac hypertrophy. Silencing of Kif5b reverted the peripheral mitochondrial localization in PE stimulated NRVCs and diminished PE induced increases in mitochondrial OCR, indicating that KIF5B dependent localization affects cellular responses to PE stimulated NRVCs. These results indicate that KIF5B contributes to mitochondrial localization and function in cardiomyocytes and may play a role in pathological hypertrophic responses in vivo.

2016-04-21 | GSE73896 | GEO

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