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Gene expression in experimental aortic coarctation and repair: candidate genes for therapeutic intervention?

ABSTRACT: The objective of the current investigation was to use microarray techniques to quantify differentially expressed genes (DEGs) in the upstream aorta subjected to high arterial BP after surgical induction of CoA, and restoration of normal arterial BP after its correction. DEGs may offer additional insight into potential mechanisms of persistent CV morbidity despite successful surgical repair.

ORGANISM(S): Oryctolagus cuniculus

PROVIDER: GSE70687 | GEO | 2015/07/10

SECONDARY ACCESSION(S): PRJNA289362

REPOSITORIES: GEO

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Gene expression in experimental aortic coarctation and repair: candidate genes for therapeutic intervention?

Project description:The objective of the current investigation was to use microarray techniques to quantify differentially expressed genes (DEGs) in the upstream aorta subjected to high arterial BP after surgical induction of CoA, and restoration of normal arterial BP after its correction. DEGs may offer additional insight into potential mechanisms of persistent CV morbidity despite successful surgical repair. Male New Zealand white rabbits ~10 weeks old and weighing ~1.0 kg randomly underwent proximal dAo CoA. A 20 mmHg BP gradient was imposed using silk (permanent) or Vicryl (degradable) suture to mimic untreated CoA and surgically corrected CoA, respectively. Rabbits develop a pronounced stenosis and accompanying elevated BP as a stimulus for arterial remodeling within one week. Degradation of Vicryl suture in the corrected group restores aortic diameter close to normal, but with modest residual narrowing. Non-experimental rabbits were designated as a control group. This results in a statistically significant increase in mean, systolic and pulse BP proximal to the coarctation for CoA as compared to both control and corrected rabbits. A ~4 mm circumferential region from the proximal aorta between the coarctation site and left subclavian artery was excised at harvest (32 weeks of age) and frozen. Frozen samples (n=4/group) were shipped overnight to Arraystar, Inc (Rockville, MD) for microarray analysis.

2015-07-10 | E-GEOD-70687 | biostudies-arrayexpress

Gene Expression in Experimental Aortic Coarctation and Repair: Candidate Genes for Therapeutic Intervention?

Project description: Not available

| S-EPMC4514739 | biostudies-literature

Cycloastragenol inhibit experimental abdominal aortic aneurysm progression

Project description:Abstract: The pathogenesis of AAA involves vascular inflammation and oxidative stress. Astragali Radix contains cycloastragenol (CAG) known to have anti-inflammatory and anti-oxidative properties. We hypothesized that CAG supplement impairs AAA progression. AAA was induced in male rats by intraluminal elastase infusion in the infrarenal aorta and treated daily with CAG (125 mg/kg/day). Aortic expansion was followed weekly by ultrasound, with euthanization at day 28. Changes in AAA wall composition were analyzed at mRNA levels, histology, zymography and explorative proteomic analyses. At day 28, mean AAA diameter was 37% lower in CAG group (p<0.0001). In aneurysm cross sections, elastin content was insignificantly higher in CAG group (10.5% ± 5.9% vs 19.9% ± 16.8%, p=0.20) with more preserved elastin lamellae structures (p=0.0003) and with no microcalcifications. Aneurysmal matrix metalloprotease-2 activity was reduced by CAG treatment (p=0.022), and mRNA levels of inflammatory- and antioxidative markers showed no difference between groups. Explorative proteomic analysis showed no difference in protein levels when adjustment for multiple testing. Amongst unadjusted affected proteins were fibulin-5 (p=0.02), aquaporin-1 (p=0.02) and prostacyclin synthase (p=0.006). CAG impairs experimental AAA progression by reduction of elastin degradation through decreased MMP-2 activity, thus CAG could be considered tested in AAA patients.

2022-05-20 | PXD030441 | Pride

Abdominal Aortic Aneurysm in C57BL/6J Mice - Male and Female PPE vs. Sham Day 7

Project description:Transcriptional profiling of infrarenal aorta from male and female mice (10-weeks old, C57BL/6J), treated with either porcine pancreatic elastase (PPE) local infusion or sham operation (saline infusion). Samples harvested 7 days after treatment. Goal was to examine gene expression in AAA in this model in both genders. Surgical protocol is as described in PMCID: PMC3148686/PMID: 19629030.

2022-03-03 | GSE197748 | GEO

Aortic extracellular space components

Project description:THORACIC AORTA GUANIDINE EXTRACT

2012-07-20 | PRD000269 | Pride

The VE-cadherin/AmotL2 mechanosensory pathway suppresses aortic inflammation and the formation of abdominal aortic aneurysms

Project description:Arterial endothelial cells (ECs) have the ability to respond to mechanical forces exerted by laminar fluid shear stress. This response is of importance, as it is protective against vascular diseases such as atherosclerosis and aortic aneurysms. Mechanical forces are transmitted at the sites of adhesion to the basal membrane as well as cell-cell junctions where protein complexes connect to the cellular cytoskeleton to relay force into the cell. Here we present a novel protein complex that connects junctional VE-cadherin and radial actin filaments to the LINC complex in the nuclear membrane. We show that the scaffold protein AmotL2 is essential for the formation of radial actin filaments and the flow-induced alignment of aortic endothelial cells. The deletion of endothelial AmotL2 alters nuclear shape as well as subcellular positioning. Molecular analysis shows that VE-cadherin is mechanically associated with the nuclear membrane via binding to AmotL2 and Actin. Furthermore, the deletion of AmotL2 in ECs provoked a pro-inflammatory response and abdominal aortic aneurysms (AAA) in the aorta of mice on a normal diet. Remarkably, transcriptome analysis of AAA samples from human patients revealed a negative correlation between AmotL2 expression and inflammation of the aortic intima. These findings provide a conceptual framework regarding how mechanotransduction in the junctions is coupled with vascular diseases.

2023-08-21 | PXD042661 | Pride

RhoBTB1 Reverses Established Arterial Stiffness in Angiotensin II Hypertension

Project description:We are investigating of role of RhoBTB1 in vascular smooth muscle cells. Restoring RhoBTB1 expression in mouse aorta reversed the established arterial stiffness but not hypertension caused by angiotensin II (Ang-II). To investigate the underlying mechanism by which RhoBTB1 reversed arterial stiffness, we performed bulk RNA-sequencing using aorta from four groups: control /RhoBTB1 transgenic mice treated with/without Ang-II.

2022-04-08 | GSE189003 | GEO

Epigenome analysis of ascending aorta from normal, aortic dissection and bicuspid aortic valve patients

Project description:Genome wide DNA methylation profiling of ascending aorta tissue samples from normal, aortic dissection and bicuspid aortic valve patients with aortic dilation. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across more than 450,000 CpGs in ascending aorta samples. Samples included 6 normal donors, 12 patients with aortic dissection and 6 patients with bicuspid aortic valve and dilated aorta.

2019-07-11 | GSE84274 | GEO

Expression data from Aortic Macrophages

Project description:Normal arteries contain a large population of tissue resident macrophages (MÎ¦). Their origins, as well as the mechanisms that sustain them during homeostasis and disease, however, are poorly understood. Gene expression profiling, we show, identifies arterial MÎ¦ as a distinct population among tissue MÎ¦. Ontologically, arterial MÎ¦ arise before birth, though CX3CR1-, Csf1r-, and Flt3-driven fate mapping approaches demonstrate MÎ¦ colonization occurs through successive contributions of yolk sac (YS) and conventional hematopoiesis. In adulthood, arterial MÎ¦ renewal is driven by local proliferation rather than monocyte recruitment from the blood. Proliferation sustains MÎ¦ not only during steady state conditions, but mediates their rebound after severe depletion following sepsis. Importantly, the return of arterial MÎ¦ to functional homeostasis after infection is rapid; repopulated MÎ¦ exhibit a transcriptional program similar to resting MÎ¦ and efficiently phagocytose bacteria. Collectively, our data provide a detailed framework for future studies of arterial MÎ¦ function in health and disease. Aortic macrophages (CD11bhighF4/80highCD45+MerTK+CD64+) were isolated from C57/B6 wild-type male mice aged 6-8 weeks before and 7 days after induction of sepsis by cecal puncture. 18-20 aortas were pooled per sample. Each condition contained three biological replicates.

2015-12-07 | E-GEOD-68968 | biostudies-arrayexpress

Expression data from Aortic Macrophages

Project description:Normal arteries contain a large population of tissue resident macrophages (MΦ). Their origins, as well as the mechanisms that sustain them during homeostasis and disease, however, are poorly understood. Gene expression profiling, we show, identifies arterial MΦ as a distinct population among tissue MΦ. Ontologically, arterial MΦ arise before birth, though CX3CR1-, Csf1r-, and Flt3-driven fate mapping approaches demonstrate MΦ colonization occurs through successive contributions of yolk sac (YS) and conventional hematopoiesis. In adulthood, arterial MΦ renewal is driven by local proliferation rather than monocyte recruitment from the blood. Proliferation sustains MΦ not only during steady state conditions, but mediates their rebound after severe depletion following sepsis. Importantly, the return of arterial MΦ to functional homeostasis after infection is rapid; repopulated MΦ exhibit a transcriptional program similar to resting MΦ and efficiently phagocytose bacteria. Collectively, our data provide a detailed framework for future studies of arterial MΦ function in health and disease.

2015-12-07 | GSE68968 | GEO

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