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Left ventricular hypertrophy and metabolic resetting in the Notch3-deficient adult mouse heart

ABSTRACT: Left ventricular hypertrophy and metabolic resetting in the Notch3-deficient adult mouse heart

PROVIDER: PRJNA993615 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25232419.fastq.gz	Fastqsanger.gz
	SRR25232420.fastq.gz	Fastqsanger.gz
	SRR25232421.fastq.gz	Fastqsanger.gz
	SRR25232422.fastq.gz	Fastqsanger.gz
	SRR25232423.fastq.gz	Fastqsanger.gz

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Left ventricular hypertrophy and metabolic resetting in the Notch3-deficient adult mouse heart

Project description:The heart depends on a functional vasculature for oxygenation and transport of nutrients, and while occlusion of the coronary arteries can lead to myocardial infarction, it remains less explored how a more subtle primary impairment of the vasculature can indirectly affect cardiac function and morphology of the heart. Notch3-deficiency causes vascular smooth muscle cell (VSMC) loss in the vasculature but the consequences for the heart remain largely elusive. Here, we demonstrate that Notch3-/- mice have enlarged hearts with left ventricular hypertrophy and mild fibrosis. Cardiomyocytes were hypertrophic but not hyperproliferative, and the expression of several cardiomyocyte markers, including TnT2, MYH6, MYH7 and Actn2, was altered. Furthermore, expression of genes regulating the metabolic status of the heart was altered: both Pdk4 and Cd36 were downregulated, indicating a metabolic switch from fatty acid oxidation to glucose consumption. Notch3-/- mice furthermore showed lower liver lipid content. Notch3 was expressed in heart VSMC and pericytes but not in cardiomyocytes, suggesting that a perturbation of Notch signalling in VSMC and pericytes indirectly impairs the cardiomyocytes. In keeping with this, Pdgfbret/ret mice, characterized by reduced numbers of VSMC and pericytes, showed left ventricular and cardiomyocyte hypertrophy. In conclusion, we demonstrate that reduced NOTCH3 or PDGFB signalling in vascular mural cells lead to cardiomyocyte dysfunction.

2023-09-21 | GSE237040 | GEO

NHLBI TOPMed: HyperGEN: Genetics of Left Ventricular Hypertrophy

Project description:NHLBI TOPMed: HyperGEN: Genetics of Left Ventricular Hypertrophy

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NHLBI TOPMed: HyperGEN - Genetics of Left Ventricular (LV) Hypertrophy

Project description:<p>The Hypertension Genetic Epidemiology Network Study (HyperGEN) - Genetics of Left Ventricular (LV) Hypertrophy is a familial study aimed to understand genetic risk factors for LV hypertrophy by conducting genetic studies of continuous traits from echocardiography exams. The originating HyperGEN study aimed to understand genetic risk factors for hypertension. Data from detailed clinical exams as well as genotyping data for linkage studies, candidate gene studies and GWAS have been collected and is shared between HyperGEN and the ancillary HyperGEN - Genetics of LV Hypertrophy study.</p>

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MicroRNAs in an Experimental Model of Physiologic Left Ventricular Hypertrophy: a Microarray-based Analysis

Project description:BACKGROUND - MicroRNAs (miRs) are a class of small non-coding RNAs that regulate gene expression. Transgenic models have proved that a single miR can induce pathological cardiac hypertrophy and failure. The roles of miRs in the genesis of physiologic left ventricular hypertrophy (LVH), however, are not well elucidated. OBJECTIVE - To evaluate miRs expression in an experimental model of exercise-induced LVH. METHODS - Male Balb/c mice were divided into sedentary (SED) and exercise (EXE) groups. Voluntary exercise was performed in odometer-monitored metal wheels during 35 days. Analyses were performed after 7 and 35 days of training, and consisted of transthoracic echocardiography, maximal exercise test, miRs microarray (miRBase v.16) and real-time qRT-PCR analysis. RESULTS - Left ventricular weight/body weight ratio increased by 7% in the EXE group at day 7 (p<0.01) and by 11% at 35 days of training (p<0.001) After 7 days of training, microarray identified 35 deregulated miRs: 20 had an increase in their expression and 15 were down-regulated (p=0.01). At day 35 of training, 25 miRs were deregulated: 15 were up-regulated and 10 had decreased their expression compared to the SED group (p<0.01). qRT-PCR confirmed an increase in miR-150 levels at both time points and a decrease in miR-26b, miR-27a and miR-143 after 7 days of voluntary exercise. CONCLUSIONS M-bM-^@M-^S We unraveled new miRs that can modulate physiological cardiac hypertrophy, particularly miR-26b, -150, 27a and -143. Our data also indicate that previously established regulatory gene pathways involved in pathological LVH are not deregulated in physiologic LVH. Experimental model of left ventricular hypertrophy induced by voluntary exercise Male Balb/c mice, 8-10 weeks old, 4 groups analyzed, each group consisted of a pool from 4 animals

2014-06-01 | E-GEOD-52278 | biostudies-arrayexpress

Left ventricular hypertrophy and metabolic resetting in the Notch3-deficient adult mouse heart.

Project description:The heart depends on a functional vasculature for oxygenation and transport of nutrients, and it is of interest to learn how primary impairment of the vasculature can indirectly affect cardiac function and heart morphology. Notch3-deficiency causes vascular smooth muscle cell (VSMC) loss in the vasculature but the consequences for the heart remain largely elusive. Here, we demonstrate that Notch3-/- mice have enlarged hearts with left ventricular hypertrophy and mild fibrosis. Cardiomyocytes were hypertrophic but not hyperproliferative, and the expression of several cardiomyocyte markers, including Tnt2, Myh6, Myh7 and Actn2, was altered. Furthermore, expression of genes regulating the metabolic status of the heart was affected: both Pdk4 and Cd36 were downregulated, indicating a metabolic switch from fatty acid oxidation to glucose consumption. Notch3-/- mice furthermore showed lower liver lipid content. Notch3 was expressed in heart VSMC and pericytes but not in cardiomyocytes, suggesting that a perturbation of Notch signalling in VSMC and pericytes indirectly impairs the cardiomyocytes. In keeping with this, Pdgfbret/ret mice, characterized by reduced numbers of VSMC and pericytes, showed left ventricular and cardiomyocyte hypertrophy. In conclusion, we demonstrate that reduced Notch3 or PDGFB signalling in vascular mural cells leads to cardiomyocyte dysfunction.

| S-EPMC10497627 | biostudies-literature

Transcription profiling of 5 heart chambers of mice 20 days after Thoracic Aortic Constriction (TAC) which led to left atrial enlargement and left ventricular hypertrophy

Project description:15 ug RNA isolated from 5 heart chambers of mice 20 days after Thoracic Aortic Constriction which led to left atrial enlargement and left ventricular hypertrophy was used to prepare labeled cDNA for test channel, 15ug of RNA from whole e17.5 mouse embryos used to prepare labeled cDNA for reference channel. 3 biological replicates were performed for eash tissue. Diseased chamber tissue was compared to sham operated control tissue.

2005-01-01 | E-SMDB-24 | biostudies-arrayexpress

Ribo-seq of murine left ventricular tissues

Project description:To evaluate the genome-wide changes in gene translational efficiency during the development of heart failure, we performed transverse aortic constriction(TAC) in male C57BL/6 mice. According to our experience, hypertrophy of the left ventricle was observed 2 weeks after TAC. Cardiac decompensation was observed at 5 weeks. We collected left ventricular tissues at 0, 2, 5 weeks after TAC and then performed ribosome footprinting and sequencing.

2023-10-31 | E-MTAB-8552 | biostudies-arrayexpress

MicroRNAs in an Experimental Model of Physiologic Left Ventricular Hypertrophy: a Microarray-based Analysis

Project description:BACKGROUND - MicroRNAs (miRs) are a class of small non-coding RNAs that regulate gene expression. Transgenic models have proved that a single miR can induce pathological cardiac hypertrophy and failure. The roles of miRs in the genesis of physiologic left ventricular hypertrophy (LVH), however, are not well elucidated. OBJECTIVE - To evaluate miRs expression in an experimental model of exercise-induced LVH. METHODS - Male Balb/c mice were divided into sedentary (SED) and exercise (EXE) groups. Voluntary exercise was performed in odometer-monitored metal wheels during 35 days. Analyses were performed after 7 and 35 days of training, and consisted of transthoracic echocardiography, maximal exercise test, miRs microarray (miRBase v.16) and real-time qRT-PCR analysis. RESULTS - Left ventricular weight/body weight ratio increased by 7% in the EXE group at day 7 (p<0.01) and by 11% at 35 days of training (p<0.001) After 7 days of training, microarray identified 35 deregulated miRs: 20 had an increase in their expression and 15 were down-regulated (p=0.01). At day 35 of training, 25 miRs were deregulated: 15 were up-regulated and 10 had decreased their expression compared to the SED group (p<0.01). qRT-PCR confirmed an increase in miR-150 levels at both time points and a decrease in miR-26b, miR-27a and miR-143 after 7 days of voluntary exercise. CONCLUSIONS – We unraveled new miRs that can modulate physiological cardiac hypertrophy, particularly miR-26b, -150, 27a and -143. Our data also indicate that previously established regulatory gene pathways involved in pathological LVH are not deregulated in physiologic LVH.

2014-06-01 | GSE52278 | GEO

Renalase Alleviates Left Ventricular Hypertrophy and Fibrosis in a Chronic Kidney Disease Mouse Model

Project description:Renalase Alleviates Left Ventricular Hypertrophy and Fibrosis in a Chronic Kidney Disease Mouse Model

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The SRSF4/lncRNA GAS5 axis regulates left ventricular hypertrophy by inhibiting the glucocorticoid receptor

Project description:The SRSF4/lncRNA GAS5 axis regulates left ventricular hypertrophy by inhibiting the glucocorticoid receptor

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