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Gene expression profiling of human-derived primary cardiomyocytes with lncRNA ZNF593-AS 5‘ end overexpression under phenylephrine stimulation

ABSTRACT: Gene expression profiling of human-derived primary cardiomyocytes with lncRNA ZNF593-AS 5‘ end overexpression under phenylephrine stimulation

PROVIDER: PRJNA686998 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13282321_1.fastq.gz	Fastqsanger.gz
	SRR13282321_2.fastq.gz	Fastqsanger.gz
	SRR13282322_1.fastq.gz	Fastqsanger.gz
	SRR13282322_2.fastq.gz	Fastqsanger.gz
	SRR13282323_1.fastq.gz	Fastqsanger.gz

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Gene expression profiling of human-derived primary cardiomyocytes with lncRNA ZNF593-AS 5‘ end overexpression under phenylephrine stimulation

Project description:The aim of this study is to investigate molecular mechanisms underlying the function of lncRNA ZNF593-AS in cardiomyocyte under phenylephrine stimulation in vitro.

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

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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

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The translational landscape of phenylephrine-treated neonatal rat cardiomyocytes

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Expression dada in adult mouse cardiomyocytes with knockdown of Hoxa5 (ID:15402) or not and treated with phenylephrine (100μM)

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

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

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

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

Project description:The translational landscape of phenylephrine-treated neonatal rat cardiomyocytes [Ribo-seq]

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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

2016-06-30 | E-GEOD-82339 | biostudies-arrayexpress

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

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