Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA89995 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2021-05-05 | PXD022309 | Pride
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2018-04-24 | PXD007288 | Pride
Project description:Ascending thoracic aortopathy is a life-threatening disease significantly influenced by angiotensin II (AngII). Thoracic aortopathy exhibits regional heterogeneity with the ascending region being susceptible. Smooth muscle cells (SMCs), a major component of the aortic wall, originate from two embryonic origins in the ascending aorta: second heart field (SHF) and cardiac neural crest (CNC). However, functional differences between the origins in AngII-induced thoracic aortopathy formation remain unknown. The present study determined transcriptomic differences between origins in response to AngII by single-cell RNA sequencing using the lineage tracing approach. Mef2c-Cre +/0 mT/mG mice were infused with AngII (1,000 ng/kg/day). To investigate causative mechanisms, ascending aortas were harvested after 3 days of AngII infusion, representing the prepathological phase of thoracic aortopathy. Aortic samples were also harvested from Mef2c-Cre +/0 mT/mG mice without AngII infusion as a control. Following single-cell suspension, cells were sorted based on their origin using mTotamto and mGFP signals. mGFP proteins were present on Mef2c-Cre-driven cells indicating the cells were derived from the SHF, while cells with mTomato signal were not derived from the SHF (nSHF). After sorting cells by origin, single-cell RNA sequencing was performed. Two-way ANOVA analysis identified 1718 differentially expressed genes (DEGs) in the interaction between origin and infusion. Among these DEGs, 1207 genes significantly differed between origins in response to AngII infusion. However, the magnitude of difference in most of these DEGs was modest, ranging between −0.05 and 0.05 Log2FC. Commonly studied molecules, such as TGF-β, SMC contraction, and extracellular matrix molecules, were undetectable or modestly different. In conclusion, transcriptomic differences in SMCs between origins in response to AngII were modest in the pre-pathological phase of AngII-induced thoracic aortopathy.
2025-01-01 | GSE275132 | GEO
Project description:Obesity-induced secretory disorder of adipose tissue-derived factors is important for cardiac damage. However, whether platelet-derived growth factor-D (PDGF-D), a newly identified adipokine, regulates cardiac remodeling in Angiotensin II (AngII)-infused obese mice is unclear. Here, we found obesity induced PDGF-D expression in adipose tissue, as well as more severe cardiac remodeling compared to control lean mice after AngII infusion. Adipocyte-specific PDGF-D knockout attenuated hypertensive cardiac remodeling in obese mice. Consistently, adipocyte-specific PDGF-D overexpression transgenic mice (PA-Tg) showed exacerbated cardiac remodeling after AngII infusion without high-fat diet treatment. Mechanistic studies indicated that AngII-stimulated macrophages produce urokinase plasminogen activator (uPA) that activates PDGF-D by splicing full-length PDGF-D into the active PDGF-DD. Moreover, bone marrow specific uPA knockdown decreased active PDGF-DD level in the heart and improved cardiac remodeling in HFD hypertensive mice. Together, our data provide for the first time a new interaction pattern between macrophage and adipocyte, that macrophage-derived uPA activates adipocyte-secreted PDGF-D, which finally accelerates AngII-induced cardiac remodeling in obese mice.
2021-05-27 | GSE175572 | GEO
Project description:Introgressed variants from other species can be an important source of genetic variation because they may arise rapidly, can include multiple mutations on a single haplotype, and have often been pretested by selection in the species of origin. Although introgressed alleles are generally deleterious, several studies have reported introgression as the source of adaptive alleles-including the rodenticide-resistant variant of Vkorc1 that introgressed from Mus spretus into European populations of Mus musculus domesticus. Here, we conducted bidirectional genome scans to characterize introgressed regions into one wild population of M. spretus from Spain and three wild populations of M. m. domesticus from France, Germany, and Iran. Despite the fact that these species show considerable intrinsic postzygotic reproductive isolation, introgression was observed in all individuals, including in the M. musculus reference genome (GRCm38). Mus spretus individuals had a greater proportion of introgression compared with M. m. domesticus, and within M. m. domesticus, the proportion of introgression decreased with geographic distance from the area of sympatry. Introgression was observed on all autosomes for both species, but not on the X-chromosome in M. m. domesticus, consistent with known X-linked hybrid sterility and inviability genes that have been mapped to the M. spretus X-chromosome. Tract lengths were generally short with a few outliers of up to 2.7 Mb. Interestingly, the longest introgressed tracts were in olfactory receptor regions, and introgressed tracts were significantly enriched for olfactory receptor genes in both species, suggesting that introgression may be a source of functional novelty even between species with high barriers to gene flow.
| S-EPMC8784167 | biostudies-literature
Project description:In order to study the capacity of the myocardium to recover from a stress causing several features of heart failure with preserved ejection fraction, C57Bl6/J male and female mice received or not for 28 days an angiotensin II (AngII; 1,5 mg/kg/day) continuous infusion in combination with a high fat diet (HFD). Half of the animals were then euthanized. The remaining ones had the AngII infusion stopped and their diet normalized. In addition, voluntary exercise was initiated by introducing a running wheel in the animals cage for an additional 28 days.
2023-12-18 | GSE240171 | GEO
Project description:Dicer conditional knockout embryonic heart mutant vs control array
| PRJNA100449 | ENA
Project description:Translational research is commonly performed in the C57B6/J mouse strain, chosen for its genetic homogeneity and phenotypic uniformity. Here, we evaluate the suitability of the white-footed deer mouse (Peromyscus leucopus) as a model organism for aging research, offering a comparative analysis against C57B6/J and diversity outbred (DO) Mus musculus strains. Our study includes comparisons of body composition, skeletal muscle function, and cardiovascular parameters, shedding light on potential applications and limitations of P. leucopus in aging studies. Notably, P. leucopus exhibits distinct body composition characteristics, emphasizing reduced muscle force exertion and a unique metabolism, particularly in fat mass. Cardiovascular assessments showed changes in arterial stiffness, challenging conventional assumptions and highlighting the need for a nuanced interpretation of aging-related phenotypes. Our study also highlights inherent challenges associated with maintaining and phenotyping P. leucopus cohorts. Behavioral considerations, including anxiety-induced responses during handling and phenotyping assessment, pose obstacles in acquiring meaningful data. Moreover, the unique anatomy of P. leucopus necessitates careful adaptation of protocols designed for Mus musculus. While showcasing potential benefits, further extensive analyses across broader age ranges and larger cohorts are necessary to establish the reliability of P. leucopus as a robust and translatable model for aging studies.
| S-EPMC11335981 | biostudies-literature
Project description:Physiological and pathological stimuli result in distinct anatomic forms of cardiac hypertrophy, but the head-to-head comparison of molecular regulation between physiological and pathological cardiac hypertrophy is less well understood, especially at the DNA methylation level. We conducted an in vitro study using human cardiomyocyte cell line AC16 exposed to angiotensin II (AngII) and insulin-like growth factor 1 (IGF-1) to mimic pathologically and physiologically hypertrophic heart models, respectively. Whole genome DNA methylation patterns were profiled by the Infinium human MethylationEPIC platform with >850K DNA methylation loci. We detected 194 loci that are significantly differentially methylated after AngII treatment (vs control) with 50.0% hypermethylated, and 206 significant loci after IGF-1 treatment (vs control) with 45.1% hypermethylated (Adjusted P < 0.05). Mapping the significant loci to genes, we identified 158 genes corresponding to AngII treatment and 175 genes to IGF-1 treatment, with 67 genes overlapping between AngII and IGF-1.
2023-10-03 | GSE241551 | GEO