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Gene expression profiling in thoracic aortas of 8 week and 16 week ApoE knockout mice on a western type diet

ABSTRACT: Identification of novel pathways in the development of atherosclerosis. Here, we are looking at changes in gene expression that occur in the aorta with the development of atherosclerosis

ORGANISM(S): Mus musculus

PROVIDER: GSE65494 | GEO | 2015/02/03

SECONDARY ACCESSION(S): PRJNA274260

REPOSITORIES: GEO

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Gene expression profiling in thoracic aortas of 8 week and 16 week ApoE knockout mice on a western type diet

Project description:Identification of novel pathways in the development of atherosclerosis. Here, we are looking at changes in gene expression that occur in the aorta with the development of atherosclerosis Analysis used RNA from thoracic aortas from chow fed ApoE knockout mice as control samples for comparison to the experimental samples from 8 week and 16 week ApoE knockout mice fed a western-type diet

2015-02-03 | E-GEOD-65494 | biostudies-arrayexpress

Identification of Key Genes Associated with Macrophage Autophagy in ApoE-/- Mice Atherosclerosis by Aortic Gene Expression Profile

Project description:This study aimed to investigate genes associated with the development of atherosclerosis in the aorta of ApoE-/- mice

2024-01-04 | GSE232472 | GEO

Transcription profiling of mouse smooth muscle cells in atherosclerosis-prone and resistant regions of the aorta of apoE-/- mice at age of 4 months

Project description:This study compared gene expression in smooth muscle cells (SMCs) in atherosclerosis-prone and atherosclerosis-resistant aorta segments in 4 months old apolipoprotein E-deficient (apoE-/-) mice before plaque development. In a parallel experiment, both regions were compared in young C57Bl/6 mice. Aortas of 3 male and 3 female ApoE-/- 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 a resistant region (TA: central thoracic aorta, i.e. 6 mm distal from the proximal 2 mm). Microarray analysis (VIB-MAF) of pooled total RNA showed differential expression (>2-fold difference) for 244 genes. Up- or downregulation in the AA was observed for 186 and 58 genes respectively. Differential expression of 6 genes was confirmed using real-time PCR. The 201 genes that showed exclusively differential expression in apoE-/- mice were related to processes involved in atherosclerosis, such as cell adhesion, proliferation, differentiation, motility and death, lipid metabolism and immune responses. Furthermore, the transcription profile of the AA was in accordance with a more synthetic SMC phenotype. These results point to an altered transcriptome in SMCs in the aorta of apoE-/- mice at the atherosclerosis-prone location before actual lesion development. This suggests that SMCs, in addition to endothelial cells, can facilitate plaque formation at predilection sites. Experiment Overall Design: samples were hyrbidized in dye-swap.

2009-05-27 | E-GEOD-13836 | biostudies-arrayexpress

Smooth muscle cells in atherosclerosis-prone and resistant regions of the aorta of apoE-/- mice at age of 4 months

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Effects of TREM-1 pharmacological blockade within aortas of apoE KO mice

Project description:mouse aorta

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Microarray gene expression profiling of aorta genes of APOE-deficient mice receiving the ACE inhibitor captopril

2009-12-03 | GSE19286 | GEO

Expression data from the aortas of ApoE knockout and ApoE/IL-17 double knockout mice

Project description:Interleukin-17 (IL-17)-secreting T helper 17 cells (Th17) are a recently identified CD4+ T helper subset that has been implicated in various inflammatory and autoimmune diseases. The issue of whether interleukin-17A (IL-17) contributes to hyperlipidemia-induced aortic endothelial cell activation remained unknown. Here, we reported that IL-17 contributes to hyperlipidemia-induced modulation of vascular cell gene expression during early atherosclerosis in vivo. Our results has shed lights onto the role of IL-17 on EC biology and has provided important insights for future development of novel therapeutics for early intervention of cardiovascular diseases and other inflammatory diseases.

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Transcription profiling of mouse aorta genes of APOE-deficient animals receiving the ACE inhibitor captopril

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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Descending thoracic aorta perivascular adipocytes adipogenesis is defined by their anatomical location

Project description:Hypertension, atherosclerosis, and aneurysms alter thoracic aorta structure. Aortic lesions found in these diseases show a unique anatomical distribution. For instance, calcifications and atherosclerotic lesions tend to occur more frequently in the posterior wall of the aorta compared to other regions. The role that the outer layer of the aorta, its perivascular adipose tissue (PVAT), plays in the pathogenesis of these lesions is unknown. The descending thoracic aorta's PVAT is distributed in three strips of tissue: one strip is located anterior to the aorta (AP), while the other two are positioned laterally to the vessel and are adjacent to the thoracic vertebrae (LP). Genetic tracing indicates LP's adipocytes descend from sm22a+ and Myf5+ progenitors while the anterior are from sm22a+ only. The implications of this ontology and aortic PVAT distribution on the development of adipocytes are unknown. We hypothesize that the anatomical location of adipocyte progenitors influences their adipogenic potential. PVAT from LP and AP was collected from male SD rats at 10 wks of age (n=7) to harvest progenitors by outgrowth expansion. Progenitors were differentiated for 4 d in adipogenic media. Adipogenesis was evaluated by lipid droplet and triglyceride quantification using the IncuCyte Live-Cell® system. RNA from progenitors and adipocytes was sequenced in Illumina NextSeqData, and Differential Expressed Genes (DEG) identified. Enrichment and network analyses were performed in Ingenuity Pathways (IPA). Our findings provide evidence supporting differences in adipogenic activity and extracellular matrix secretion between the LP and AP PVAT of the aorta. These differences may explain the anatomical location of aortic lesions associated with hypertension, atherosclerosis, and aneurysms.

2023-10-11 | GSE244664 | GEO

Expression data from the aortas of ApoE knockout, ApoE/Caspase-1 double knockout, and wild-type mice

Project description:Caspase-1 activation senses metabolic danger-associated molecular patterns and mediates the initiation of inflammation. Here, we reported that caspase-1 contributes to hyperlipidemia-induced modulation of vascular cell gene expression during early atherosclerosis in vivo. Our results demonstrate the therapeutic potential of caspase-1 inhibition in the treatment of cardiovascular diseases.

2015-08-21 | GSE72248 | GEO

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