Ontology highlight
ABSTRACT:
PROVIDER: PRJNA986702 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25024072_1.fastq.gz | Fastqsanger.gz | |||
| SRR25024072_2.fastq.gz | Fastqsanger.gz | |||
| SRR25024073_1.fastq.gz | Fastqsanger.gz | |||
| SRR25024073_2.fastq.gz | Fastqsanger.gz | |||
| SRR25024074_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
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Project description:We tried to identify miRs that are differentially expresssed during atherogenesis. Aortic miRs expression profile in female apoe-/- mice after 3 and 10 months of a high fat diet were compared with female apoe-/- mice on normal diet. 4 Female apoe-/- mice (6-8 weeks) were fed on high fat diet for 3 months. 3 female apoe-/- mice (6-8 weeks) were fed on high fat diet for 10 months. 4 female apoe-/- mice (6-8 weeks) on normal diet served as controls. Total RNA was isolated from whole aortic tissue. RNA samples with RIN>8 were used for array. The aortic miRs expression profile after 3 months of a high fat diet was compared with the control group. Biological replicates: 4 per group. One replicate per array.
2014-01-01 | E-GEOD-26557 | biostudies-arrayexpress
Project description:We found that hyperglycemia and elevated fatty acids in diabetes could activate protein kinase C-β isoforms and selectively induce insulin resistance via inhibiting vascular insulin signaling. To further investigate the effect of high fat diet and specific PKC β inactivation on STZ-induced atherosclerosis using the PKC β inhibitor, ruboxistaurin (RBX, or LY333531), ApoE-/- mice were used and fed with high fat diet (42% of fat Kcal) with or without RBX after onset of diabetes. Isolated total RNA from whole aortas of each group was used and analyzed for gene expression. The gene expression profiles were processed by using the Microarray Suite version 5.0 (MAS 5.0) with Affymetrix default analysis settings. ApoE-/- mice were used as a rodent atherosclerosis model. Isolated total RNA from aortas of each ApoE-/- mouse fed with high fat diet for 10 weeks after STZ-induced diabetes or control groups were used for preparation and hybridization on Affymetrix microarrays. There were total 4 different mice groups, which were fed with high fat diet with or without RBX. Each group had four individual mouse (N=4).
2016-03-26 | E-GEOD-79623 | biostudies-arrayexpress
Project description:CD45+CD11b+ cells from the whole aortas of ApoE-/- and ApoE-/- Clec4a2-/- mice fed a high fat diet (HFD) for 12 weeks using using 10X genomics platform (9 mice in each genotype were pooled; one experiment).
2021-10-28 | E-MTAB-10746 | biostudies-arrayexpress
Project description:This series represents a comparison of gene expression in mouse aorta from MyD88-/-, apoE-/- mice versus apoE-/- control mice fed a high fat diet for 8 weeks, causing atherosclerotic lesion development. 5 MyD88-/-, apoE-/- mice were compared to 5 apoE-/- control mice and dye swap replicated for a total of 10 replicate microarrays. Keywords = Mus musculus Keywords = aorta Keywords = atherosclerosis Keywords = MyD88
2010-06-09 | E-GEOD-1058 | biostudies-arrayexpress
Project description:Aortic arch profiling of Apoe-/- mice fed a high fat diet (HFD, Harlan Teklad 88137, 21% fat, 0.15% cholesterol) starting at 8 weeks of age for 8, 16, and 24 weeks. B6 mice fed HFD for 16 weeks starting at 8 weeks of age were used as controls. Apoe-/- mice were fed a high fat diet (HFD, Harlan Teklad 88137, 21% fat, 0.15% cholesterol) starting at 8 weeks of age for 8, 16, and 24 weeks. B6 mice fed HFD for 16 weeks starting at 8 weeks of age were used as controls. At each time point, 9 mice were studied. Mice were euthanized at each time point and whole aorta (from aortic root to renal bifurcation) of each mouse was immediately collected and flash-frozen in liquid N2. Mice were fasted overnight prior to euthanasia. the aortic arches of three mice in the same study group were pooled, resulting in three pools per study group.
2010-06-22 | E-GEOD-18443 | biostudies-arrayexpress
Project description:We developed a novel network inference approach, Biologically Anchored Knowledge Expansion (BAKE), to analyze large volume gene expression data obtained from a mouse model of insulin resistance progression. Both genetic aspects and dietary factors, specifically high caloric high-fat high-sugar diets, contribute to the progression of insulin resistance. To mimic genetic predisposition, we used a mouse model with double heterozygous deletion of early insulin signaling pathway intermediates, insulin receptor (IR) and insulin receptor substrate 1 (IRS1) genes. These mice were fed with high-fat (Western) or low-fat (Chow) diet for 8 and 16 weeks starting at 8 weeks of age. Gene expression data was collected from adipocytes isolated from these mice. Applying BAKE analysis to the adipocyte gene expression data, we demonstrate that we can accurately discover a novel regulatory gene in the insulin signaling pathway. The mouse model of double heterozygous deletion of insulin receptor (IR) and insulin receptor substrate 1 (IRS1) was originally introduced as a polygenic model to study the development of type 2 diabetes. This mouse model, on an atherosclerosis-prone ApoE null background (IR+/- IRS1+/- ApoE-/-), also shows increased atherosclerotic lesions due to impaired insulin signaling. For our study we used female double heterozygous mice (IR+/- IRS1+/-, 'Dhet' mice or 'Dâ mice) on an ApoE null background (ApoE-/-, âEâ) fed with a Western (high-fat) diet for 8 (DW8, n=5) and 16 (DW16, n=9) weeks starting at 8 weeks of age or with a Chow (low-fat) diet (DC8, n=7; DC16, n=5). There were also ApoE null mice (ApoE-/-, 'Eâ) fed either Western diet for 8 (EW8, n=6) and 16 (EW16, n=8) weeks or Chow diet for 16 weeks (EC16, n=5) starting at 8 weeks of age.
2015-12-31 | E-GEOD-76428 | biostudies-arrayexpress
Project description:Chronic kidney disease (CKD) can induce AoSMCs premature senescence and phenotypic switching, which ultimately promotes AS progression and plaque vulnerability. However, the underlying mechanisms are still unknown. To identify the underlying mechanisms of AoSMCs senescence and phenotype switching in CKD. We performed integrated microarray analysis of AoSMCs from normal-diet fed ApoE-/- (ND) mice, high fat-fed ApoE-/- (AS) mice and CKD ApoE-/- (accelerated atherosclerosis mouse model, AAS) mice.
2019-08-10 | GSE135626 | GEO
Project description:Aortic arch profiling of Apoe-/- mice fed a high fat diet (HFD, Harlan Teklad 88137, 21% fat, 0.15% cholesterol) starting at 8 weeks of age for 8, 16, and 24 weeks. B6 mice fed HFD for 16 weeks starting at 8 weeks of age were used as controls.
2010-06-23 | GSE18443 | GEO
Project description:This series represents a comparison of gene expression in mouse aorta from MyD88-/-, apoE-/- mice versus apoE-/- control mice fed a high fat diet for 8 weeks, causing atherosclerotic lesion development. 5 MyD88-/-, apoE-/- mice were compared to 5 apoE-/- control mice and dye swap replicated for a total of 10 replicate microarrays. Keywords = Mus musculus Keywords = aorta Keywords = atherosclerosis Keywords = MyD88 Keywords: other
2004-02-26 | GSE1058 | GEO