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Transcriptome-wide microRNA expression of the heart of neonatal rats with polygenic cardiac hypetrophy

ABSTRACT: Identification of microRNAs differentially expressed between the neonatal heart of a genetic rat model of cardiac hypertrophy (the Hypertrophic Heart Rat, HHR) and the control (the Normal Heart Rat, NHR) using the Agilent Rat miRNA Microarray Kit Release 16.0.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE38710 | GEO | 2017/12/01

SECONDARY ACCESSION(S): PRJNA168489

REPOSITORIES: GEO

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Transcriptome-wide microRNA expression of the heart of neonatal rats with polygenic cardiac hypetrophy

Project description:Identification of microRNAs differentially expressed between the neonatal heart of a genetic rat model of cardiac hypertrophy (the Hypertrophic Heart Rat, HHR) and the control (the Normal Heart Rat, NHR) using the Agilent Rat miRNA Microarray Kit Release 16.0. Neonatal (day 2) HHR and age-matched NHR were killed with an overdose of pentobarbitone (Lethobarb). The heart was immediately removed, and the ventricles were dissected from the atriums. The tissues were first preserved in liquid nitrogen and later transferred to a M-bM-^@M-^S80C freezer. Microarrays (one per sample, with no pooling) were performed on 8 neonatal HHR (4 male, 4 female) and 8 neonatal NHR (4 male, 4 female). After extraction of RNA, cRNA was prepared and arrays performed using Agilent Rat miRNA Microarray Kit Release 16.0 performed at the Ramaciotti Gene Function Analysis facility, University of New South Wales in Sydney, Australia.

2014-02-03 | E-GEOD-38710 | biostudies-arrayexpress

Transcriptome-wide gene expression of the heart of neonatal rats with polygenic cardiac hypetrophy

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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

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

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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.

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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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Binding Profiles of Myc and RNA Polymerase II in Rat Neonatal Cardiomyocytes

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Deubiquitinase USP29 Ameliorates Pathological Cardiac Hypertrophy Through Inhibiting TAK1

Project description:The identification of key factors involved in pathological cardiac hypertrophy is crucial to exploring novel treatments for heart failure. In this study, we elucidated the role of Ubiquitin-specific protease 29 (USP29), a deubiquitinase, in pressure overload-induced cardiac hypertrophy. Genetic knockout of USP29 in mice significantly exacerbated TAC-induced heart hypertrophy, dysfunction, and fibrosis; whereas overexpression of USP29 in cardiomyocytes attenuated the hypertrophic response. Similarly, USP29 markedly alleviated PE-induced hypertrophy of primary neonatal rat cardiomyocytes. Mechanistically, the cardio-protective effects mediated by USP29 were attributed to its suppression of transforming growth factor β-activated kinase 1 (TAK1)-JNK/P38 signaling pathway activation. Collectively, our study suggests that targeting either USP29 or its interaction with TAK1 could represent an innovative therapeutic strategy for treating heart failure and cardiac hypertrophy.

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Project description:Cardiac hypertrophy has been well-characterized at the level of transcription. During cardiac hypertrophy, genes normally expressed primarily during fetal heart development are re-expressed, and this fetal gene program is believed to be a critical component of the hypertrophic process. Recently, alternative splicing of mRNA transcripts has been shown to be temporally regulated during heart development, leading us to consider whether fetal patterns of splicing also reappear during hypertrophy.We hypothesized that patterns of alternative splicing occurring during heart development are recapitulated during cardiac hypertrophy. Here we present a whole-transcriptome study of isoform expression during pressure-overload cardiac hypertrophy induced by 10 days of transverse aortic constriction (TAC) in rats and in developing fetal rat hearts compared to sham-operated adult rat hearts, using high-throughput sequencing of poly(A) tail mRNA. Quantification of isoform expression in fetal rat hearts, pressure-overloaded rat hearts, and sham-operated rat hearts by Illumina GAIIx in triplicate

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Targeting Cytoplasmic SAM by Expressing Slc25a26 Inhibits Protein Synthesis in Cardiac Hypertrophy via SAMTOR/mTOR signaling

Project description:Excess protein synthesis is the major pathological manifestation of cardiac hypertrophy; however, the underlying mechanism remains elusive. Here we found that a SAM transporter Slc25a26 translocated to mitochondria during cardiac hypertrophy. Silencing Slc25a26 aggravated phenylephrine-induced cardiomyocyte hypertrophy in neonatal rat ventricular myocytes. Transcriptome analysis revealed a specific regulation of ribosome genes by Slc25a26. Puromycin incorporation assay showed a negative regulation of protein synthesis rate by Slc25a26. The translational regulation was independent of ribosome assembly, but abolished by mTOR inhibitor rapamycin. Administration of SAM, or silencing Samtor, reversed the inhibitory impact of Slc25a26 on protein synthesis. AAV9-mediated Slc25a26 overexpression in mouse heart increased the SAM level in mitochondria, but reduced that in nucleus and cytoplasm. Transaortic-constriction-induced hypertrophic pathologies, including pathological gene induction, cardiomyocyte enlargement, myocardial remodeling and heart dysfunction were significantly alleviated by Slc25a26 overexpression. Our data demonstrate a crucial role of subcellular SAM homeostasis in translational control during cardiac hypertrophy.

2022-01-05 | GSE173737 | GEO

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