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

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE82339 | GEO | 2016/06/30

SECONDARY ACCESSION(S): PRJNA324677

REPOSITORIES: GEO

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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

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

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

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 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

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

miRNA 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 through altered miRNA activity, 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 siRNA for KChIP2 and subsequently performed miRNA microarray analysis to identify up-regulation of potential miRNA targets.

2017-02-20 | GSE75806 | GEO

siRNA knockdown in neonatal rat cardiac myocytes

Project description:Primary neonatal rat cardiac myocytes were isolated and subjected to siRNA mediated Yap knockdown

2019-07-04 | GSE121929 | GEO

Slc39a2-mediated Zinc Homeostasis Modulates Innate Immune Signaling in Phenylephrine-induced Cardiomyocyte Hypertrophy

Project description:Zinc dyshomeostasis has been involved in the pathogenesis of cardiac hypertrophy; however, the dynamic regulation of intracellular zinc and its downstream signaling in cardiac hypertrophy remain largely unknown. Here we screened ZIP (SLC39) family members that were responsible for zinc uptake in a phenylephrine (PE)-induced cardiomyocyte hypertrophy model. We found that Slc39a2 was the only member that was altered at mRNA level by PE treatment in neonatal rat ventricular myocytes (NRVMs), but its protein level was not affected. Zincpyr1 staining showed a significant decrease in zinc uptake after PE treatment or after Slc39a2 knockdown in NRVMs, indicating an inhibition of its transport activity during hypertrophy. Slc39a2 deficiency caused spontaneous hypertrophy in NRVMs, and further exacerbated the hypertrophic responses after PE treatment. RNA sequencing analysis confirmed a largely aggravated pro-hypertrophic transcriptome reprogramming after Slc39a2 knockdown. Interestingly, the innate immune pathways, including NOD signaling, TOLL-like receptor, NFB, and IRFs, were substantially enriched after Slc39a2 knockdown. Whereas IRF7, the most sensitive among all IRFs, did not mediate the effect of Slc39a2 in hypertrophy, pro-hypertrophy phosphorylations of NFB and STAT3 were significantly enhanced after Slc39a2 knockdown, in parallel with degradation of IkBα protein. Our data demonstrate that SLC39A2-mediated zinc homeostasis contributes to the remodeling of innate immune signaling in cardiomyocyte hypertrophy, and provide novel insights into the pathogenesis of heart failure and its treatment.

2021-11-24 | GSE175884 | GEO

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