Unknown,Transcriptomics,Genomics,Proteomics

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Circulating microRNA profiling by array in dogs with myxomatous mitral valve degeneration (MMVD) and pulmonic stenosis (PS) compared with healthy dogs

ABSTRACT: In this study, we aimed to demonstrate expression profiles of circulating microRNAs (miRNAs) in dogs with eccentric or concentric cardiac hypertrophy, and investigate whether there is a difference in miRNA expression according to the type of cardiac hypertrophy. Dogs with myxomatous mitral valve degeneration (MMVD) or pulmonic stenosis (PS) were included in this study, which are the two representative diseases of eccentric or concentric cardiac hypertrophy in dogs, respectively. Circulating miRNAs were isolated from the serum samples of five dogs with MMVD, five dogs with PS, and five healthy dogs. The circulating miRNA expression levels of dogs with MMVD or PS were compared with those of the healthy dogs by microarray analysis (Affymetrix GeneChip miRNA 4.0), using two independent parameters, a fold change cut-off of > 1.5 (up or down regulation) and p-value of < 0.05.

ORGANISM(S): Canis lupus familiaris

SUBMITTER: Woong-Bin Ro

PROVIDER: E-MTAB-10029 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Aims: We investigate sex differences and the role of oestrogen receptor beta (ERbeta) in a mouse model of pressure overload-induced myocardial hypertrophy. Methods and results: We performed transverse aortic constriction (TAC) or sham surgery in male and female wild-type (WT) and ER knockout (ERbeta-/-) C57Bl6 mice. All mice were characterised by echocardiography and haemodynamic measurements and were sacrificed nine weeks after surgery. Left ventricular (LV) samples were analysed by microarray profiling, real-time RT-PCR and histology. After nine weeks, WT males showed more hypertrophy and heart failure signs than WT females. Notably, WT females developed a concentric form of hypertrophy, while males developed eccentric hypertrophy. These sex differences were abolished in ERbeta-/- mice. ERbeta deletion augmented the TAC-induced increase in cardiomyocyte diameter in both sexes. Gene expression profiling revealed that male WT hearts had a stronger induction of matrix-related genes and a stronger repression of mitochondrial genes than female hearts. ERbeta-/- mice exhibited a different transcriptome. Induction of pro-apoptotic genes after TAC occurred in ERbeta-/- mice of both sexes with a stronger expression in ERbeta-/- males. Histological analysis revealed, that cardiac fibrosis was more pronounced in male WT TAC than in female mice. This was abolished in ERbeta-/- mice. Apoptosis was significantly induced in both sexes of ERbeta-/- TAC mice, but it was most prominent in males. Conclusion: Female sex offers protection against ventricular chamber dilation in the TAC model. Both the female sex and ER attenuate the development of fibrosis and apoptosis; thus slowing the progression to heart failure. The influence of sex (male/female) and estrogen receptor beta expression (ERbeta knockout/wildtype) on cardiac hypertrophy (transverse aortic constriction/sham operated) was investigated. The left ventricular transcriptome of four individual mice for each combination of the three factors (sex, genotype, surgery) was detected with Affymetrix RAE 430 2.0 GeneChip arrays.

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Circulating microRNA profiling by array in dogs with myxomatous mitral valve degeneration (MMVD) and pulmonic stenosis (PS) compared with healthy dogs

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