Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA183457 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Hypercholesterolemic APOE-deficient mice are a widely used experimental model of atherosclerosis and increased generation of reactive oxygen species (ROS) is a prominent feature of atherosclerosis development. To study the impact of ROS on atherogenesis, we treated APOE-deficient mice for 7 months with the antioxidant vitamin E (2000 IU/kg diet) and performed whole genome microarray gene expression profiling of aortic genes. Microarray gene expression profiling was performed of whole aortas isolated from vitamin E-treated APOE-deficient relative to untreated APOE-deficient mice with overt atherosclerosis, and nontransgenic B6 control mice. Microarray gene expression profiling revealed that vitamin E treatment prevented atherosclerosis-related gene expression changes of the aortic intima and media. Microarray gene expression profiling was performed of whole aortas isolated from APOE-deficient mice with atherosclerosis relative to vitamin E-treated APOE-deficient mice, and nontransgenic B6 control mice. Three study groups were analyzed, i.e. 8 months-old untreated APOE-deficient mice with overt atherosclerosis, age-matched APOE-deficient mice treated for 7 months with the antioxidant vitamin E (2000 IU/kd diet), and nontransgenic B6 control (C57BL/6J) mice. Two biological replicates were made of each group, and total RNA of three aortas was pooled for one gene chip. The study complements microarray study GSE19286.
2012-12-11 | E-GEOD-42813 | biostudies-arrayexpress
Project description:Hypercholesterolemic APOE-deficient mice are a widely used experimental model of atherosclerosis and increased generation of reactive oxygen species (ROS) is a prominent feature of atherosclerosis development. To study the impact of ROS on atherogenesis, we treated APOE-deficient mice for 7 months with the antioxidant vitamin E (2000 IU/kg diet) and performed whole genome microarray gene expression profiling of aortic genes. Microarray gene expression profiling was performed of whole aortas isolated from vitamin E-treated APOE-deficient relative to untreated APOE-deficient mice with overt atherosclerosis, and nontransgenic B6 control mice. Microarray gene expression profiling revealed that vitamin E treatment prevented atherosclerosis-related gene expression changes of the aortic intima and media.
2012-12-11 | GSE42813 | GEO
Project description:Microarray gene expression profiling of aorta genes of APOE-deficient mice receiving atherosclerosis treatment with the ACE inhibitor captopril. Hypercholesterolemic APOE-deficient mice were used as a standard model of atherosclerosis to study gene expression changes during atherosclerosis treatment with the ACE inhibitor captopril. Microarray analysis was performed of whole aortas isolated from captopril-treated APOE-deficient mice relative to untreated APOE-deficient mice with overt atherosclerosis, and nontransgenic control mice. Microarray gene expression profiling revealed that captopril-mediated atherosclerosis prevention involved inhibition of aorta-infiltrating immune cells such as pro-atherogenic T lymphocytes and macrophages.
2009-12-03 | GSE19286 | GEO
Project description:Microarray gene expression profiling of aorta genes of APOE-deficient mice receiving atherosclerosis treatment with the ACE inhibitor captopril. Hypercholesterolemic APOE-deficient mice were used as a standard model of atherosclerosis to study gene expression changes during atherosclerosis treatment with the ACE inhibitor captopril. Microarray analysis was performed of whole aortas isolated from captopril-treated APOE-deficient mice relative to untreated APOE-deficient mice with overt atherosclerosis, and nontransgenic control mice. Microarray gene expression profiling revealed that captopril-mediated atherosclerosis prevention involved inhibition of aorta-infiltrating immune cells such as pro-atherogenic T lymphocytes and macrophages. Experiment Overall Design: Microarray gene expression profiling was performed of whole aortas isolated from APOE-deficient mice with atherosclerosis relative to captopril-treated APOE-deficient mice, and nontransgenic control mice. Three study groups were analyzed, i.e. 8-months-old untreated APOE-deficient mice with overt atherosclerosis, age-matched APOE-deficient mice treated for 7 months with the angiotensin-converting enzyme (ACE) inhibitor, captopril (20 mg/kg in drinking water), and nontransgenic control C57BL/6J mice. Two biological replicates were made of each group, and total RNA of three aortas was pooled for one gene chip.
2009-12-14 | E-GEOD-19286 | biostudies-arrayexpress
Project description:Strain differences influence susceptibility to atherosclerosis. Apolipoprotein E-null mice on a DBA/2J genetic background (DBA-apoE) and C57BL/6 (B6-apoe) are highly susceptible to atherosclerosis in the aortic root area compared with those on a 129S6/SvEvTac background (129-apoE). To explore strain-specific differences affecting the susceptibility to atherosclerosis, we performed microarray analysis of aortic arch and root from wild type mice of each strains.
2014-12-01 | GSE52818 | GEO
Project description:Atherosclerosis and pressure overload are major risk factors for the development of heart failure in patients. Cardiac hypertrophy often precedes the development of heart failure. However, underlying mechanisms are incompletely understood. To investigate pathomechanisms underlying the transition from cardiac hypertrophy to heart failure we used experimental models of atherosclerosis- and pressure overload-induced cardiac hypertrophy and failure, i.e. apolipoprotein E (apoE)-deficient mice, which develop heart failure at an age of 18 months, and non-transgenic C57BL/6J (B6) mice with heart failure triggered by 6 months of pressure overload induced by abdominal aortic constriction (AAC). The development of heart failure was monitored by echocardiography, invasive hemodynamics and histology. The microarray gene expression study of cardiac genes was performed with heart tissue from failing hearts relative to hypertrophic and healthy heart tissue, respectively. The microarray study revealed that the onset of heart failure was accompanied by a strong up-regulation of cardiac lipid metabolism genes involved in fat synthesis, storage and oxidation. Microarray gene expression profiling was performed with heart tissue isolated from (i) 18 month-old apoE-deficient mice relative to age-matched non-transgenic C57BL/6J (B6) mice, (ii) 6 month-old apoE-deficient mice with 2 months of chronic pressure overload induced by abdominal aortic constriction (AAC) relative to sham-operated apoE-deficient mice and nontransgenic B6 mice, (iii) 10 month-old B6 mice with 6 months of AAC relative to sham-operated B6 mice, and (iv) 5 month-old B6 mice with 1 month of AAC relative to age-matched B6 mice.
2010-12-03 | E-GEOD-25765 | biostudies-arrayexpress
Project description:Inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) exhibit a marked difference in their susceptibility to atherosclerosis and the arterial wall has proven to be a source of the difference in atherosclerosis susceptibility. Genome-wide gene expression analysis was conducted in aortic walls of the two strains. Total RNA was extracted from aortas of 6-week-old female B6 and C3H apoE-deficient (apoE-/-) mice fed a chow or Western diet. 1514 genes in chow fed mice and 590 genes in Western fed mice were found to be differentially expressed between the two strains. RNA was extracted from aorta using a Trizol protocol. Total RNA was pooled in an equal amount from 4 mice for each group. Standard Affymetrix procedures were performed using 8ug of total RNA. Microarrays were used to detect gene expression in aortic walls of two apoE-deficient mouse strains when fed a chow or western diet. Experiment Overall Design: 4 groups of mice were studied: C57BL/6 apoE-/- mice on chow diet (03-62_BC), C57BL/6 apoE-/- mice on Western diet (03-62_BW), C3H/HeJ apoE-/- mice on chow diet (03-62_CC), and C3H/HeJ apoE-/- mice on Western diet (03-62_CW). Mice were weaned at 3 weeks of age onto a chow diet. At 4 weeks of age, mice were switched onto a western diet or continued the chow diet for 2 additional weeks.
2009-02-28 | E-GEOD-14854 | biostudies-arrayexpress
Project description:Inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) exhibit a marked difference in their susceptibility to atherosclerosis and the arterial wall has proven to be a source of the difference in atherosclerosis susceptibility. Genome-wide gene expression analysis was conducted in aortic walls of the two strains. Total RNA was extracted from aortas of 6-week-old female B6 and C3H apoE-deficient (apoE-/-) mice fed a chow or Western diet. 1514 genes in chow fed mice and 590 genes in Western fed mice were found to be differentially expressed between the two strains. RNA was extracted from aorta using a Trizol protocol. Total RNA was pooled in an equal amount from 4 mice for each group. Standard Affymetrix procedures were performed using 8ug of total RNA. Microarrays were used to detect gene expression in aortic walls of two apoE-deficient mouse strains when fed a chow or western diet. Keywords: atherosclerosis, arterial walls, C57BL/6, C3H/HeJ, Inbred strains, Hyperlipidemia, and Western diet
2009-02-20 | GSE14854 | GEO
Project description:Strain differences influence susceptibility to atherosclerosis. Apolipoprotein E-null mice on a C57BL/6 genetic background (B6-apoE) are highly susceptible to atherosclerosis in the aortic root area compared with those on a 129S6/SvEvTac background (129-apoE). To explore strain-specific differences affecting the susceptibility to atherosclerosis, we performed microarray analysis of macrophages from wild type mice of each strains.
2014-12-01 | GSE52816 | GEO
Project description:Strain differences influence susceptibility to atherosclerosis. Apolipoprotein E-null mice on a DBA/2J genetic background (DBA-apoE) are highly susceptible to atherosclerosis in the aortic root area compared with those on a 129S6/SvEvTac background (129-apoE). To explore strain-specific differences affecting the susceptibility to atherosclerosis, we performed microarray analysis of macrophages from wild type mice of each strains.
2014-12-01 | GSE52473 | GEO