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Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of neonatal rat ventricular myocytes treated with phenylephrine or PAMH

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Eric Olson

PROVIDER: E-GEOD-925 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Canonical transient receptor potential channels promote cardiomyocyte hypertrophy through activation of calcineurin signaling.

Bush Erik W EW Hood David B DB Papst Philip J PJ Chapo Joseph A JA Minobe Wayne W Bristow Michael R MR Olson Eric N EN McKinsey Timothy A TA

The Journal of biological chemistry 20060901 44

The calcium/calmodulin-dependent phosphatase calcineurin plays a central role in the control of cardiomyocyte hypertrophy in response to pathological stimuli. Although calcineurin is present at high levels in normal heart, its activity appears to be unaffected by calcium during the course of a cardiac cycle. The mechanism(s) whereby calcineurin is selectively activated by calcium under pathological conditions has remained unclear. Here, we demonstrate that diverse signals for cardiac hypertrophy ...[more]

PMID: 16950785

Similar Datasets

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

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

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

2016-06-30 | GSE82339 | GEO

RNA-seq transcriptonal profiling in neonatal rat ventricular myocytes under hypertrophic growth

Project description:Heart failure is a leading cause of death in US. Hypertension is one of the most important risk factor of heart failure. In the presence of high blood pressure, the heart manifests hypertrophic growth to ameliorate ventricular wall stress. This once adaptive response may progress into decompensation and heart failure. The precise mechanisms governing this transition remain elusive. Here, we aimed to identify novel signaling pathways in cardiac hypertrophic growth. Primary neonatal rat ventricular myocytes (NRVMs) were isolated from 1-2 days old rats and treated with phenylephrine or IGF-1. Total RNA was isolated for RNA-seq analysis.

2020-11-16 | GSE153763 | GEO

Transcription profiling of rat neonatal ventricular myocytes

Project description:Title: Regulation of gene expression through mitogen-activated protein kinase cascades in cardiac myocytes. Description: The aim of this study is to identify the changes in gene expression induced in rat neonatal ventricular myocytes, a well-established cell culture model, by endothelin-1, a known hypertrophic agonist, and to determine which of the changes are mediated through the ERK cascade. This continues TKAC^Ys previous study of the effects of oxidative stress, which induces cardiac myocyte apoptosis.

2006-10-01 | E-MIMR-3 | biostudies-arrayexpress

Transcription profiling of rat neonatal ventricular myocytes plated in fibronectin reveals fibronectin induced cardiac myocyte hypertrophy

Project description:Gene expression changes in neonatal rat ventricular myocytes plated in fibronectin (2 samples) or uncoated plates (2 samples).

2008-06-11 | E-GEOD-1055 | biostudies-arrayexpress

Transcription profiling of phenylepherine response in rat neonatal ventricular myocytes

Project description:Title: Regulation of gene expression through mitogen-activated protein kinase cascades in cardiac myocytes. Description: We aim to identify the changes in gene expression induced in rat neonatal ventricular myocytes, a well established cell culture model, by phenylepherine, a known hypertrophic agonist, and to determine which of the changes are mediated through the ERK cascade. In addition, we intend to extend the previous studies (EXP_TKAC_0102_01 and EXP_TKAC_1103_02) on endothelin-1 induced hypertrophy and the oxidative stress induced by H2O2 by using additional concentrations and timepoints.

2006-10-01 | E-MIMR-37 | biostudies-arrayexpress

JIP1 knockout in PE and TSA treated NRVMS

Project description:Jip1 was knocked out in neonatal rat ventricular myocytes in the presence of phenylephrine and trichostatin a

2018-03-21 | GSE102609 | GEO

Transcription profiling of neonatal rat ventricular cardiac myocytes treated with interleukin 33 for 0.5, 1 or 2 hours

Project description:Study of the effect of interleukin 33 (IL33) on transcript expression in neonatal rat ventricular cardiac myocytes at 0.5, 1 or 2 h

2010-04-01 | E-MEXP-1912 | biostudies-arrayexpress

Whole-transcriptome expression data from neonatal rat ventricular myocytes (NRVM) silenced for KChIP2

Project description:Loss of KChIP2 during cardiac stress has been suggested to have a transcriptional impact on cardiac ion channels contributing to maladaptive electrical remodeling. Therefore, we tested the consequence of KChIP2 loss, in the absence of cardiac stress, by treating cultured neonatal rat ventricular myocytes with shRNA for KChIP2 and subsequently performed whole-transcriptome microarray analysis to identify gene changes.

2017-02-20 | GSE94623 | GEO

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