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Cpxm2 as a novel candidate for cardiac hypertrophy and failure in hypertension [Affymetrix]

ABSTRACT: Cpxm2 as a novel candidate for cardiac hypertrophy and failure in hypertension [Affymetrix]

PROVIDER: PRJNA645893 | ENA |

REPOSITORIES: ENA

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Cpxm2 as a novel candidate for cardiac hypertrophy and failure in hypertension

Project description:Cpxm2 as a novel candidate for cardiac hypertrophy and failure in hypertension

| PRJNA645891 | ENA

Cpxm2 as a novel candidate for cardiac hypertrophy and failure in hypertension [Illumina]

Project description:Cpxm2 as a novel candidate for cardiac hypertrophy and failure in hypertension [Illumina]

| PRJNA645894 | ENA

Cpxm2 as a novel candidate for cardiac hypertrophy and failure in hypertension [Affymetrix]

Project description:We assigned carboxypeptidase X 2 (Cpxm2) to a genetic locus for left ventricular mass. The functional role of Cpxm2 was investigated in Cpxm2-deficient (KO) and wild-type (WT) mice exposed to deoxycorticosterone acetate (DOCA)-salt hypertension and control conditions (SHAM). Both WT and KO animals developed severe and similar systolic hypertension in response to DOCA. WT mice developed severe LV damage. These changes were significantly ameliorated or even normalized (i.e. ejection fraction) in KO-DOCA animals. LV transcriptome analysis in WT, but not in KO mice, showed a molecular cardiac hypertrophy/remodeling signature with significant upregulation of 1234 transcripts including Cpxm2 in response to DOCA.

2023-07-10 | GSE154321 | GEO

Terminal heart failure

Project description:Rats overexpressing the human renin and angiotensinogen genes die after seven weeks of end organ damage. They develop hypertension, heart hypertrophy and proteinuria.We compared terminal heart failure, these are indeed terminally ill to double transgenic animals suffering on hypertension, proteinuria and heart hypertrophy. In addition, Losartan-treated animals (10 mg/kg/d)showed similar physiological parameters (normotension, no proteinuria and no heart hypertrophy compared to control sprague dawley rats. Keywords: other

2005-01-03 | GSE1557 | GEO

Transcription profiling of rats with terminal heart failure and cachexia

2008-06-11 | E-GEOD-1557 | biostudies-arrayexpress

Cpxm2 as a novel candidate for cardiac hypertrophy and failure in hypertension [Illumina]

Project description:To identify novel targets in left ventricular (LV) hypertrophy (LVH) we initiated comparative transcriptome analysis between genetic models derived from stroke-prone spontaneously hypertensive rats (SHRSP) and Fischer (F344). Previous genetic studies in the SHRSP/F344 model confirmed the presence of a major quantitative trait locus (QTL) for LV mass on rat chromosome (RNO) 1. We assigned carboxypeptidase X 2 (Cpxm2) to a genetic locus for LV mass identified in SHRSP. We assigned carboxypeptidase X 2 (Cpxm2) to a genetic locus for left ventricular mass.

2023-07-10 | GSE154326 | GEO

Cardiac hypertrophy and failure

Project description:Analysis of cardiac specific AT1 transgenic mice undergoing cardiac failure, cardiac hypertrophy and wild type aged matched controls. For detailed description of the AT1 Tg mice please refer to: Paradis P, Dali-Youcef N, Paradis FW, Thibault G, Nemer M. Overexpression of angiotensin II type I receptor in cardiomyocytes induces cardiac hypertrophy and remodeling. Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):931-6. PMID: 10639182 [PubMed - indexed for MEDLINE] Keywords: ordered

2005-06-15 | GSE2355 | GEO

The tubulin code during cardiac hypertrophy and failure

Project description:The tubulin code during cardiac hypertrophy and failure

| PRJNA800418 | ENA

Transcription profiling of male and female wildtype FVB and TNF-alpha transgenic mice at the time point of compensated hypertrophy and dilated heart failure to study the molecular mechanism of heart failure.

Project description:Cardiac-specific TNF-alpha transgenic mice are an excellent model to study the pathologenesis of heart failure. Affymetrix U74V2A was used to analyze the gene expression profile of male and female wildtype FVB and TNF-alpha transgenic mice at the time point of compensated hypertrophy and dilated heart failure. 3 week, 13 week and 40 week samples examined.

2007-12-15 | E-GEOD-591 | biostudies-arrayexpress

Prdm16 deficiency leads to age-dependent cardiac hypertrophy, adverse remodeling, mitochondrial dysfunction, and heart failure

Project description:Hypertrophic cardiomyopathy (HCM) is one of the most frequent inherited heart condition and a well-established risk factor for cardiovascular mortality worldwide. Although hypertrophy is traditionally regarded as an adaptive response to increased workload caused by physiological or pathological stress, prolonged hypertrophy can lead to heart failure characterized by impaired systolic function, increased apoptosis, fibrosis, ventricular dilation, and impaired metabolic substrate flexibility. While the key regulators for cardiac hypertrophy are well studied, the role of Prdm16 in this process remains poorly understood. In the present study, we demonstrate that Prdm16 is dispensable for cardiac development. However, it is required in the adult heart to preserve mitochondrial function and inhibit hypertrophy with advanced age. Cardiac-specific deletion of Prdm16 results in cardiac hypertrophy, excessive ventricular fibrosis, mitochondrial dysfunction, and impaired metabolic flexibility, leading to heart failure. We demonstrate that Prdm16 and euchromatic histone-lysine N- methyltransferase factors (Ehmts) act together to reduce the expression of fetal genes reactivated in pathological hypertrophy by inhibiting the functions of pro- hypertrophic transcription factor Myc. Although young Prdm16 knockout mice show normal cardiac function, they are predisposed to develop heart failure in response to metabolic stress. Collectively, our results demonstrate that Prdm16 protects the heart against age-dependent cardiac hypertrophy, fibrosis, mitochondrial dysfunction, adverse metabolic remodeling, and heart failure.

2020-09-21 | GSE153988 | GEO

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