Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA189505 | ENA |
REPOSITORIES: ENA
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Project description:Time-series of gene expression in female murine ES cells during EpiSC differentiation
| PRJNA149761 | ENA
Project description:Mouse ES-cells with different sex chromosome compliment were differentiated into EpiSC, samples were taken every 4-12 hours for 84 hours in total. The original data for the XX-cells is also available as GSE34243, but normalisation of these differs.
2014-02-11 | GSE44340 | GEO
Project description:Abdominal aortic aneurysms (AAAs) are a prevalent and deadly human pathology with strong sexual dimorphism. Research demonstrates that sex hormones influence, but do not fully explain, male versus female AAA pathology. In addition to sex hormones, the X and Y sex chromosomes, and their unique complements of genes, may contribute to sexually dimorphic AAA pathology. Here, for the first time, we defined the effect of female (XX) versus male (XY) chromosome complement on AAA formation and rupture in phenotypically female mice using an established murine model. Abdominal aortas from female mice bearing the XY chromosome selectively expressed Y chromosome genes, while genes known to escape X-inactivation were higher in XX females. The majority of gene differences in XY females fell within inflammatory pathways. When XY females were infused with AngII, AAA incidences doubled and aneurysms ruptured. AAAs from XY females exhibited significant inflammation. Moreover, infusion of AngII to XY females augmented aortic activity of matrix metalloproteinases. Finally, testosterone exposure applied chronically, or as a single bolus at postnatal day 1, markedly worsened AAA outcomes in XY compared to XX females. These results demonstrate that an XY sex chromosome complement profoundly influences aortic gene expression profiles and promotes AAA severity.
2016-11-07 | GSE81580 | GEO
Project description:Sex biases in the genome-wide distribution of DNA methylation and gene expression levels are some of the manifestations of sexual dimorphism in mammals. To advance our understanding of the mechanisms that contribute to sex biases in DNA methylation and gene expression, we conducted whole genome bisulfite sequencing (WGBS) as well as RNA-seq on liver samples from mice with different combinations of sex phenotype and sex-chromosome complement. We compared groups of animals with different sex phenotypes, but the same genetic sexes, and vice versa, same sex phenotypes, but different sex-chromosome complements. We also compared sex-biased DNA methylation in mouse and human livers. Our data show that sex phenotype, X-chromosome dosage, and the presence of Y chromosome shape the differences in DNA methylation between males and females. We also demonstrate that sex bias in autosomal methylation is associated with sex bias in gene expression, whereas X-chromosome dosage-dependent methylation differences are not, as expected for a dosage-compensation mechanism. Furthermore, we find partial conservation between the repertoires of mouse and human genes that are associated with sex-biased methylation, an indication that gene function is likely to be an important factor in this phenomenon.
2022-11-14 | GSE217666 | GEO
Project description:Neural induction of ES by Retinoic acid Keywords: development or differentiation design,time series design
2006-01-23 | GSE4075 | GEO
Project description:Neural induction of ES by N2B27 monolayer culture Keywords: development or differentiation design,time series design
2006-01-23 | GSE4076 | GEO
Project description:Time series serum stimulation of ES cells of different Srf genotype
| PRJNA90897 | ENA
Project description:It is well recognized that men and women differ in circulating lipid profiles and consequently coronary artery disease (CAD). While sex hormones like estrogens are thought to protect women from CAD risk by promoting protective lipid profiles, hormone replacement therapy in women paradoxically increases CAD risk. Biological sex is determined by both sex chromosomes and sex hormones. We used mouse models to separate effects of sex chromosomes and hormones on atherosclerosis, circulating lipids and intestinal fat metabolism. We found that an XX sex chromosome complement increases food intake, body weight, fat absorption, serum lipid concentrations and atherosclerosis in gonadal male and female mice, indicating a primary effect of sex chromosome complement. Small intestine expression of enzymes involved in lipid absorption and chylomicron assembly were increased in XX male and female mice with elevated intestinal lipids. These results reveal that an XX sex chromosome complement promotes the absorption and bioavailability of dietary fat to accelerate the development of atherosclerosis.
2019-04-17 | GSE119497 | GEO
Project description:Comparison among ES, EC, TS, NS, differentiated neural cells derived from NS and placenta in addition to ES-N2B27 neural induction. Keywords: cell type comparison design,development or differentiation design,time series design
2006-01-23 | GSE4077 | GEO
Project description:To characterize the differentiation by Sox2 KO, we performed microarray analyses of mouse ES cell line 2TS22C during the time-course being induced of Sox2 KO Keywords: development or differentiation design,time series design
2007-05-23 | GSE5895 | GEO