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IL-18 and Pressure Overload-induced Cardiac Hypertrophy

ABSTRACT: Pressure overload-induced cardiac hypertrophy was examined in IL-18 knockout and littermate control mice. Keywords: genetic modification / disease model

ORGANISM(S): Mus musculus

PROVIDER: GSE5129 | GEO | 2006/07/04

SECONDARY ACCESSION(S): PRJNA96633

REPOSITORIES: GEO

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Transcription profiling of mouse IL-18 knockouts vs. wild types treated with pressure overload to examine cardiac hypertrophy

Project description:Pressure overload-induced cardiac hypertrophy was examined in IL-18 knockout and littermate control mice. Experiment Overall Design: 4 groups with RNA pooled from 5-6 per group. Role of IL-18 on gene expression in cardiac hypertrophy induced by pressure overload (transaortic constriction)

2008-06-13 | E-GEOD-5129 | biostudies-arrayexpress

Pressure-Overload Induced Cardiac Hypertrophy

Project description:Aortic banding is an excellent model system to evaluate the process of development of left ventricular hypertrophy in response to hemodynamic stress. The Affymetrix GeneChip MgU74Av1 was used to analyze expression profiles of mice at different time points after surgical intervention for pressure-overload induced hypertrophy. More information about this model may be obtained at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/band_home.html Keywords = Pressure overload, cardiac hypertrophy Keywords: time-course

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Loss of Lin28a Attenuates Cardiac Hypertrophy Induced by Pressure Overload

Project description:Pathological cardiac hypertrophy is a major risk factor for the development of heart failure and sudden cardiac death, yet the molecular mechanism of cardiac hypertrophy is not fully understood. Recently, we found that the expression of Lin28a, a RNA-binding protein, was significantly upregulated during the early stages of cardiac hypertrophy. Interestingly, cardiac specific conditional deletion of Lin28a blunted pressure overload-induced cardiac hypertrophic responses. Given that Lin28a can bind to diverse mRNA to regulate their abundance and/or translation, we conducted RNA-seq to profile the cardiac transcriptome alteration without Lin28a under pressure overload. It showed that metabolic pathways, including glycolysis and biosynthetic pathway, were remarkedly affected. Thus, our study identifies Lin28a as a crucial regulator of cardiac hypertrophy via its role in metabolic programming.

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Pressure overload cardiac hypertrophy

Project description:Expression profiling of hearts from FVB males subjected to cardiac pressure overload by transverse aortic constriction (TAC). TAC performed on 8-10 weeks month old males and females. Hearts examined 30 weeks after surgery. Keywords: ordered

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Gene and exon expression change in cardiac hypertrophy with pressure overload

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Gene and exon expression change in cardiac hypertrophy with pressure overload

Project description:Pathological cardiac hypertrophy was induced by pressure overload on the heart. We performed genome-wide exon array experiments with left ventricles of mice with 1 week and 4 week of transverse aortic constriction (TAC). The exon level analysis revealed widespread regulation of alternative splicing and alternative polyadenylation during hypertrophy. Exon and gene expression changes were examined in 1 week and 4 week TAC-operated hearts compared to sham-operated hearts. We used C57/BL6 wildtype mice, and their left ventricles were subject to surgery (each n=2).

2011-05-01 | E-GEOD-24242 | biostudies-arrayexpress

Endogenous Muscle Atrophy F-box Regulates Pressure Overload-Induced Cardiac Hypertrophy

Project description:Muscle atrophy F-box (MAFbx) is an E3 ubiquitin ligase which plays a critical role in mediating skeletal muscle atrophy. We investigated the effect of MAFbx KO in cardiac hypertrophy in response to pressure overload. A DNA microarray analysis was conducted using total RNA prepared from wild type and MAFbx KO mouse hearts subject to transverse aortic constriction (TAC). Results provide insight into the molecular mechanism to mediate the effect of MAFbx upon pathological hypertrophy. We applied TAC to wild type and MAFbx KO mice, and extracted total RNA one week after the surgery. The gene expression profiles were examined by Affymetrix Mouse Gene ST Array.

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Kdm3a in mouse promotes pressure overload induced cardiac hypertrophy

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Endogenous Muscle Atrophy F-box Regulates Pressure Overload-Induced Cardiac Hypertrophy

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Cardiac miRNA profiling during pressure overload-induced hypertrophy in PTP1B-deficient mice

Project description:The switch from the faster α-MHC to the slower β-MHC isoform that occurs in cardiac hypertrophy is generally thought to reduce contractile performance and to contribute to functional maladaptation. This MHC switch is regulated by miRNAs and thyroid hormones in development and hypertrophy. Since exacerbated hypertrophy is observed in absence of β-MHC expression in PTP1B cKO mice, we speculated that PTP1B inactivation associated with pressure-overload hypertrophy could disrupt miRNAs homeostasis. In this dataset, expression status of 1908 mouse miRNAs was investigated and reveal that PTP1B contribute to gene silencing by mediating miRNA loading onto the RISC complex.

2022-04-04 | GSE199769 | GEO

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