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

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

PROVIDER: PRJNA819432 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18465470_1.fastq.gz	Fastqsanger.gz
	SRR18465470_2.fastq.gz	Fastqsanger.gz
	SRR18465471_1.fastq.gz	Fastqsanger.gz
	SRR18465471_2.fastq.gz	Fastqsanger.gz
	SRR18465472_1.fastq.gz	Fastqsanger.gz

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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

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