Gene expression profiling in thoracic aortas of 8 week and 16 week ApoE knockout mice on a western type diet
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ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Keith Channon
PROVIDER: E-GEOD-65494 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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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.
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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.
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Project description:This study compared gene expression in smooth muscle cells (SMCs) in atherosclerosis-prone and atherosclerosis-resistant regions of the aorta of C57Bl/6 mice. In a parallel experiment, both regions were compared in young, plaque-free apolipoprotein E-deficient (apoE-/-) mice. Aortas of 3 male and 3 female C57Bl6 mice were isolated, perfused with triton X-100 to remove endothelial cells and divided in an atherosclerosis-prone region (AA: ascending aorta, aortic arch and proximal 2 mm of thoracic aorta) and an atherosclerosis-resistant region (TA: central thoracic aorta,i.e. 6 mm distal from the proximal 2mm of the thoracic aorta). Microarray analysis (VIB-MAF) of pooled total RNA showed differential expression (>2-fold difference) for 70 genes. Up- or downregulation in the AA was observed for 33 and 37 genes respectively. Differential expression of 3 genes (ATPase, Na+/K+ transporting, beta 1 polypeptide, sarcolipin and homeo box B7) was confirmed using real-time PCR. Twenty five genes showed exclusively differential expression in C57BL6 mice. Only 7 could be linked to specific processes: development (4) and cell growth (3). The other 18 genes were all involved in different processes. Among the 45 genes showing differential expression in C57Bl/6 as well as apoE-/- mice, most were related to development (13), cell growth (8) and transcription (10). These results point to an altered transcriptome in SMCs of the C57Bl/6 aorta at an atherosclerosis-prone location. This is in agreement with findings in endothelial cells in atherosclerosis-prone regions. It could be due to biomechanical differences, for instance in wall tension or shear stress, or the different embryological origin of SMCs in AA and TA. Experiment Overall Design: Samples were hybridized in dye-swap design.
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