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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

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

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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.

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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.

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miRNA expression data from neonatal rat ventricular myocytes (NRVM) silenced for KChIP2

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siRNA knockdown in neonatal rat cardiac myocytes

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

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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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