Cardiac Sex Differences in the Transcriptome of C57 Male and Female Adult Hearts
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PROVIDER: PRJNA757428 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: The goals of this study are to compare adult male and female C57 mouse hearts transcriptome profiling (RNA-seq) to conclude cardiac sex differences at the mRNA level. Methods: mRNA profiles of adult male and female C57 mouse hearts were generated by deep sequencing, n=4 for each sex, using Illumina HiSeq2500. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: Using an optimized data analysis workflow, we mapped about 50 million sequence reads per sample to the mouse genome (build mm10) and identified 16,160 transcripts in the mouse hearts.
2021-08-25 | GSE182691 | GEO
Project description:Purpose: The goals of this study are to compare E9.5 male and female C57 mouse embryonic hearts transcriptome profiling (RNA-seq) to conclude cardiac sex differences at the mRNA level. Methods: mRNA profiles of E9.5 male and female C57 mouse embryonic hearts were generated by deep sequencing, n=4 for each sex, using Illumina HiSeq2500. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (build mm10) and identified 16,460 transcripts in the mouse hearts.
2021-08-25 | GSE182690 | GEO
Project description:Cardiac Sex Differences in the Transcriptome of C57 Male and Female E9.5 Hearts
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Project description:Male and female rats received daily injections of saline or methamphetamine for 10 days. Changes in gene expression were assessed by RNA sequencing either 24 hours or 30 days following the last injection. Methamphetamine induced changes in the myocardial transcriptome were significantly greater in female hearts than male hearts both in terms of the number of genes affected and the magnitude of the changes. The largest changes in female hearts involved genes that regulate the circadian clock (Dbp, Per3, Per2, BMal1, and Npas2) which is known to impact myocardial sensitivity to ischemia. These genes were unaffected by methamphetamine in male hearts. All changes in gene expression identified at day 11 returned to baseline by day 30. These data demonstrate that female rats are more sensitive than males to methamphetamine-induced changes in the myocardial transcriptome and that methamphetamine does not induce changes in myocardial transcription that persist long term after exposure to the drug has been discontinued.
2021-03-04 | GSE158655 | GEO
Project description:Methamphetamine Induces Sex-Dependent Changes in Gene Expression in Male and Female Hearts
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Project description:There are clinically relevant sex differences in acute and chronic pain mechanisms, but we are only beginning to understand their mechanistic basis. Transcriptome analyses of rodent whole dorsal root ganglion (DRG) have revealed sex differences, mostly in immune cells. We examined the transcriptome and translatome of the mouse DRG with the goal of identifying sex differences.
2020-08-05 | GSE155676 | GEO
Project description:We have observed that DBA/2J and C57Bl6/N mice exhibit different responses to permanent coronary artery ligation, with mice in a C57 background having about a 14-fold increase in cardiomyocyte S-phase activity as compared to DBA mice. We mapped the responsible gene to the distal arm of Chromosome 3 in the C57 background. We then RNA-Seq analyses on hearts from normal and infarcted DBA and C57 mice, with the hope of identifying candidate genes within the region of interest on the distal arm of Chromosome 3 which are differentially expressed. These genes identified Tnni3k as a potential candidate contributing to the elevated S-phase phenotype.
2022-08-19 | GSE211380 | GEO
Project description:Hearts from young (2-4 month) and moderately aged (16-18 month) C57/Bl6 male mice were subjected to i) 20 min global ischaemia, 60 min reperfusion or ii) 80 min aerobic perfusion/normoxia.
2005-12-31 | E-MEXP-496 | biostudies-arrayexpress
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.
2010-01-19 | E-GEOD-18224 | biostudies-arrayexpress
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 ERbeta 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 ERbeta attenuate the development of fibrosis and apoptosis; thus slowing the progression to heart failure.
2010-01-20 | GSE18224 | GEO