Effect of endothelial ADAM10 deficiency on the aorta in an atherosclerosis mouse model
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ABSTRACT:
PROVIDER: PRJNA861312 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20440159.fastq.gz | Fastqsanger.gz | |||
| SRR20440160.fastq.gz | Fastqsanger.gz | |||
| SRR20440161.fastq.gz | Fastqsanger.gz | |||
| SRR20440162.fastq.gz | Fastqsanger.gz | |||
| SRR20440163.fastq.gz | Fastqsanger.gz |
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Project description:Mice lacking ADAM10 in endothelial cells (Tie2Cre driven) and flox-control mice were injected with an AAV8-PCSK9 virus and put on a Western-type diet for 10 weeks to induce atherosclerosis. Aorta's (Thoracoabdominal) were isolated (removal of PVAT) and processed for RNA-sequencing.
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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
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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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.
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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.
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