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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Age Dependent Decrease in Vascular Remodeling Response in LDLr-/- mice unveils a role of Quaking in Vascular Homeostasis

ABSTRACT: Female C57Bl/6J LDLr -/- mice, aged 12 weeks (n=16) and 52 weeks (n=14), were put on western-type diet for 6 weeks before perivascular bilateral collar placement in the carotid artery. RNA was isolated from the carotid artery 6 weeks after collar placement. Snap frozen carotid arteries were pooled in four subgroups of three samples per age group in order to yield a sufficient amounts of RNA. Gene expression profiles from young and old mice were compared on spotted oligonucleotide arrays containing the 22K mouse Sigma-Compugen libarary v1. A direct hybridization was used with dye swaps for each pool. Keywords: RNA expression profiling Four pools of each strain were used. Direct hybridization design. Dye swap for each pair of samples. In total 8 arrays.

ORGANISM(S): Mus musculus

SUBMITTER: Peter 't Hoen

PROVIDER: E-GEOD-9310 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Age Dependent Decrease in Vascular Remodeling Response in LDLr-/- mice unveils a role of Quaking in Vascular Homeostasis

Project description:Female C57Bl/6J LDLr -/- mice, aged 12 weeks (n=16) and 52 weeks (n=14), were put on western-type diet for 6 weeks before perivascular bilateral collar placement in the carotid artery. RNA was isolated from the carotid artery 6 weeks after collar placement. Snap frozen carotid arteries were pooled in four subgroups of three samples per age group in order to yield a sufficient amounts of RNA. Gene expression profiles from young and old mice were compared on spotted oligonucleotide arrays containing the 22K mouse Sigma-Compugen libarary v1. A direct hybridization was used with dye swaps for each pool. Keywords: RNA expression profiling

2011-10-01 | GSE9310 | GEO

Gene expression changes accompanying vascular tortuosity

Project description:To gain insight into vascular tortuosity, we analyzed gene expression in normal and tortuous vessels. We induced vascular tortuosity in basilar artery using bilateral common carotid artery ligation in One-year old SD rats. Four weeks after the ligation, total RNA was extracted. Equal amounts of RNA from four rats were pooled and 50 ng RNA was subjected to microarray analysis. Pooled RNA from four Sham operated rats were used as a control.

2021-05-15 | GSE174455 | GEO

Changes in miR expression profile carotid plaques induced by acutely induced flow disturbances in apoe-/- mice on a high fat diet.

Project description:Atherosclerosis is causally related to disturbed flow through low and oscillatory shear stress. In order to study the miR expression profile in atherosclerotic plaques induced by disturbed flow, partial ligation of the carotid artery was performed. This procedure results acutely in severly reduced blood flow and in stenotic lesion formation within 6 weeks in apoe-/- mice on a high fat diet. We compared the miR expression profile in partially ligated left carotid arteries with the untreated right carotid artery to identify miRs which are involved in plaque formation through flow disturbances. The left carotid arteries of 6 female apoe-/- mice (6-8 weeks) were partially ligated (i.e. the external and internal carotid artery as well as the occipital artery were occluded; blood flow out of the common carotid artery occurs mainly through the superior thyroid artery). Following partial ligation the animals were fed a high fat diet for 6 weeks. Total RNA was isolated from partially ligated left carotid arteries and untreated right carotid arteries (control). MiRs expression profile of the partially ligated carotid arteries were compared with the control group. Biological replicates: 6 per group. One replicate per array.

2012-12-26 | E-GEOD-26555 | biostudies-arrayexpress

Transcription profiling of mouse offspring of crosses between hypercholesterolemic and normocholesterolemic parents LUMC-HKG-ApoE-Atherosclerosis

Project description:Enhanced prenatal fatty streak formation in human fetuses has been associated with maternal hypercholesterolemia. However, the possible roles of maternal genetic background and in utero environment on development of atherosclerosis in adult life have not been unraveled. We generated genetically identical heterozygous apoE-deficient mice offspring with a different maternal background to study the intrauterine effect of maternal genotype and associated hypercholesterolemia on the developing vascular system. As read out for increased atherosclerosis development in adult life, a constrictive collar was placed around the carotid artery to induce lesion formation. A significant increase in endothelial cell activation and damage was detected in the carotid arteries of heterozygous apoE-deficient fetuses with apoE-deficient mothers compared with offspring from wild type mothers, but no fatty streak formation was observed. Postnatally, all carotid arteries revealed normal morphology. In adult offspring with maternal apoE-deficiency, the constrictive collar resulted in severe lesion (9/10) development compared with no to only minor lesions (2/10) in offspring of wild type mothers. Microarray analysis showed no effect of maternal apoE-deficiency on gene expression in adult offspring. We conclude that maternal apoE-deficiency not only affects fetal arteries, but also increases the susceptibility for development of collar-induced atherosclerosis in adult life. Experiment Overall Design: Crossing of hypercholesterolemic female with normocholesterolemic male and vice versa, determination of susceptabilioty to atherosclerosis in offspring

2008-06-14 | E-GEOD-6134 | biostudies-arrayexpress

Offsprings of crosses between hypercholesterolemic and normocholesterolemic parents LUMC-HKG-ApoE-Atherosclerosis

2007-08-08 | GSE6134 | GEO

Expression data from the carotid artery at 2 wks after Intimal injury

Project description:Injury of the arterial endothelial lamina, also called intimal injury, usually occurs after carotid endarterectomy, peripheral artery brachytherapy, stent placement for arterial occlusive disease and balloon dilatation surgeries. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process.

2021-03-23 | GSE164050 | GEO

Genome-wide analysis of mechanosensitive genes using in vivo model of mouse carotid artery endothelium exposed to disturbed flow

Project description:Recently, we have shown that disturbed flow caused by partial ligation of mouse carotid artery rapidly induces endothelial dysfunction and atherosclerosis within two weeks. To understand the molecular mechanisms by which disturbed flow induces atherosclerosis, we carried out genome-wide microarray study using endothelial RNAs isolated from the flow-disturbed left and the contralateral right common carotid artery (LCA and RCA) in C57BL/6 mice.

2011-03-10 | GSE20741 | GEO

Changes in miR expression profile carotid plaques induced by acutely induced flow disturbances in apoe-/- mice on a high fat diet.

2012-12-26 | GSE26555 | GEO

The effects of Mycophenolate treatment on the transcriptomes of patients with symptomatic carotid artery stenosis

Project description:This study was conducted in order to assess the effects of the compound Mycophenolate mofetil (MMF), an inhibitor of the enzyme inosine monophosphate dehydroxygenase (IMPDH) with a strong cytostatic effect on T-cells, on the phenotype of human carotid artery stenosis in humans in vivo. This was done at the transcriptome level by comparing the gene expression profiles of carotid endarterectomy samples from patients with carotid artery stenosis (>70% diameter stenosis on angiography) that were randomly assigned to treatment with MMF 1000 mg (N=9) or Placebo (N=11), respectively. MMF or placebo was given for at least 2 weeks prior to undergoing carotid endarterectomy (CEA).

2009-02-01 | GSE13922 | GEO

Carnitine O-octanoyltransferase is a novel inducer of vascular calcification via promoting fatty acid metabolism and mitochondrial dysfunction

Project description:Objective – Vascular calcification is a critical pathology associated with increased cardiovascular event risk, but there are no FDA-approved anti-calcific therapies. We hypothesized and validated that an unbiased screening approach would identify novel mediators of human vascular calcification. Approach and Results – We performed an unbiased quantitative proteomics and pathway network analysis that identified increased carnitine O-octanoyltransferase (CROT) in calcifying primary human coronary artery smooth muscle cells (SMCs). Additionally, human carotid artery atherosclerotic plaques contained increased immunoreactive CROT near calcified regions. CROT siRNA reduced fibrocalcific response in calcifying SMCs. In agreement, histidine 327 to alanine point mutation inactivated human CROT fatty acid metabolism enzymatic activity and suppressed SMC calcification. CROT siRNA restored mitochondrial proteome alterations and suppressed mitochondrial fragmentation in calcifying SMCs. Lipidomics analysis of SMCs incubated with CROT siRNA revealed increased eicosapentaenoic acid, a vascular calcification inhibitor. CRISPR/Cas9-mediated Crot deficiency in low-density lipoprotein receptor-deficient mice reduced aortic and carotid artery calcification without altering bone density, or liver and plasma cholesterol and triglyceride concentrations. Conclusions – CROT is a novel inducer of vascular calcification via promoting fatty acid metabolism and mitochondrial dysfunction, as such CROT inhibition has strong potential as an anti-fibrocalcific therapy.

2021-02-26 | PXD022575 | Pride

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