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RNA-sequencing analysis reveals the different gene expression in male and female wild type and TECRL knockout mice.

ABSTRACT: Purpose: In previous study, we generated the TECRL knockout mice. The purpose of this study is to indentify the implication function of TECRL on cardiac myocytes in male and female TECRL knockout(TECRL-/-) mice compared with wild type(WT) mice. Methods: Total RNA profiles of 5 males WT mice and 5 males TECRL-/- mice, 3 females WT mice and 7 females TECRL-/- mice were generated by RNA sequencing. The first strand cDNA was synthesized using random hexamer primer and the second strand cDNA synthesis was performed using DNA PolymeraseⅠand RNase H. Results: 1249 genes were identified between TECRL-/- mice and WT mice through RNA-seq analysis. GO analysis and KEGG analysis revealed some pathways, especially lipid metabolism and Ca2+ handling were closedly related to TECRL deficiency.

ORGANISM(S): Mus musculus

PROVIDER: GSE191112 | GEO | 2024/02/08

REPOSITORIES: GEO

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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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RNA-sequencing analysis reveals the different gene expression in male and female wild type and TECRL knockout mice.

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