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After stimulation by angiotensin II, changes occur in the aortic adventitial cells

ABSTRACT: After stimulation by angiotensin II, changes occur in the aortic adventitial cells

PROVIDER: PRJNA1188500 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31408000_1.fastq.gz	Fastqsanger.gz
	SRR31408000_2.fastq.gz	Fastqsanger.gz
	SRR31407999_1.fastq.gz	Fastqsanger.gz
	SRR31407999_2.fastq.gz	Fastqsanger.gz

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After stimulation by angiotensin II, changes occur in the aortic adventitial cells

Project description:Mice were stimulated with angiotensin Ⅱ, and vascular adventitial cells were extracted for single-cell sequencing analysis. Changes of DDR2 gene before and after stimulation

2025-06-16 | GSE282397 | GEO

Sex chromosome complement defines diffuse versus focal angiotensin II-induced aortic pathology

Project description:Objective-Aortic pathologies exhibit sexual dimorphism, with aneurysms in the ascending, thoracic and abdominal aorta (AAA) exhibiting higher prevalence in males. Despite lower incidence of aortic vascular disease in women, aneurysms progress rapidly. Mechanisms for these sex differences are unclear. We defined the role of sex chromosome complement and testosterone in regional development and progression of angiotensin II (AngII)-induced vascular pathologies. Approach and Results-We used transgenic male mice expressing Sry on an autosome to create low density lipoprotein receptor (Ldlr) deficient male mice with an XY or XX sex chromosome complement. Subjects were then sham operated or orcheictomized. Transcriptional profiling on abdominal aortas from XY or XX males demonstrated1746 genes influenced by sex chromosomes, sex hormones, or an interaction. A second cohort of animals was then infused with AngII for 28 days. Diffuse aortic aneurysm pathology developed in XY AngII-infused males, while XX males developed discrete AAAs. Castration reduced all AngII-induced aortic pathologies in XY and XX males. Thoracic aortas from AngII-infused XY males, but not XX males exhibited adventitial thickening. We infused male XY and XX mice with saline or AngII and quantified mRNA abundance of key genes in thoracic versus abdominal aortas. Regional differences in mRNA abundance existed before AngII infusions, which were differentially influenced by AngII between genotypes. Prolonged AngII infusions resulted in AAA aortic wall thickening in XY males with diffuse aortic pathology, while XX males had dilated focal AAAs. Conclusions-An XY sex chromosome complement mediates diffuse aortic pathology, while an XX sex chromosome complement contributes to discrete AngII-induced AAAs.

2018-07-22 | GSE102143 | GEO

Excessive adventitial stress drives inflammation-mediated fibrosis in hypertensive aortic remodelling in mice

Project description:Hypertension induces significant aortic remodelling, often adaptive but sometimes not. To identify immuno-mechanical mechanisms responsible for differential remodelling, we studied thoracic aortas from 129S6/SvEvTac and C57BL/6 J mice before and after continuous 14-day angiotensin II infusion, which elevated blood pressure similarly in both strains. Histological and biomechanical assessments of excised vessels were similar at baseline, suggesting a common homeostatic set-point for mean wall stress. Histology further revealed near mechano-adaptive remodelling of the hypertensive 129S6/SvEvTac aortas, but a grossly maladaptive remodelling of C57BL/6 J aortas. Bulk RNA sequencing suggested that increased smooth muscle contractile processes promoted mechano-adaptation of 129S6/SvEvTac aortas while immune processes prevented adaptation of C57BL/6 J aortas. Functional studies confirmed an increased vasoconstrictive capacity of the former while immunohistochemistry demonstrated marked increases in inflammatory cells in the latter. We then used multiple computational biomechanical models to test the hypothesis that excessive adventitial wall stress correlates with inflammatory cell infiltration. These models consistently predicted that increased vasoconstriction against an increased pressure coupled with modest deposition of new matrix thickens the wall appropriately, restoring wall stress towards homeostatic consistent with adaptive remodelling. By contrast, insufficient vasoconstriction permits high wall stresses and exuberant inflammation-driven matrix deposition, especially in the adventitia, reflecting compromised homeostasis and gross maladaptation.

2024-10-16 | GSE279588 | GEO

Illumina microarray analysis of three subpopulations of murine aortic adventitial cells freshly sorted by MACS, based on expression of Sca-1 and CD45

Project description:Comparison of gene expression between aortic adventitial Sca-1+CD45+ progenitor cells and Sca-1-CD45+ or Sca-1+CD45- cells. The hypothesis tested was that Sca-1+CD45+ cells would differentially express genes relating to angiogenesis and vasculogenesis when compared to Sca-1-CD45+ leukocytes.

2019-03-06 | GSE127852 | GEO

Myoblast stimulation with angiotensin II

Project description:Quiescent C2C12 myoblasts and myoblasts that were stimulated with Angiotensin II for 12 h or 24 h Keywords = Angiotensin II

2004-07-28 | E-GEOD-1592 | biostudies-arrayexpress

Angiotensin II induced aneurysms in male ApoE mice

Project description:In this study we used microarrays to examine relative genes expression within the aorta of ApoE-/- infused with angiotensin II in relation to aneurysm formation. Infusion of angiotensin II induces aortic dilatation particularly of the suprarenal aorta in ApoE-/- mice. Based on studies carried out in our and other laboratories the response to angiotensin II is variable, with some mice developing large aneurysms but other animals appearing resistant to aneurysm formation with aortic diameters similar to that of saline controls. We compared RNA expression from whole aortas of 17 week old male ApoE-/- mice exposed to angiotensin II (1.44 Âµg/kg/min) for 4 weeks where there was clear evidence of aortic aneurysm formation (n=5) with that of mice failing to develop aneurysms (n=7) and those exposed to saline infusion (n=6). AAA was defined as diameter of suprarenal aorta greated than 1.5mm measured on photographs of aortas at necroscopy. Keywords: Disease state analysis 18 samples analysed, AAA (n=5), no AAA (n=7), saline (n=6). AAA - abdominal aortic aneurysm

2010-06-24 | E-GEOD-12591 | biostudies-arrayexpress

Myoblast stimulation with angiotensin II

Project description:Quiescent C2C12 myoblasts and myoblasts that were stimulated with Angiotensin II for 12 h or 24 h Keywords = Angiotensin II Keywords: parallel sample

2004-07-28 | GSE1592 | GEO

Gene expression profiling of aortic media after long-term treatment with an angiotensin II-receptor blocker, Losartan

2010-09-23 | GSE18298 | GEO

Gene expression profiling of aortic media after long-term treatment with an angiotensin II-receptor blocker, Losartan

Project description:Rats (Wag/Rij, females) were chronically treated with Losartan (20mg/d), an angiotensin II-receptor blocker during 9 months. Gene expression profiling was performed on aortic media to understand the long-term effect of this molecule on the cardiovascular system. Two-conditions experiment, Ctrl vs Losartan-treated animals. Biological replicates: 5 control replicates, 5 Losrtan-treated animals. All the RNA samples were pooled to provide a reference RNA for a two-color experiment.

2010-09-23 | E-GEOD-18298 | biostudies-arrayexpress

Angiotensin II induced aneurysms in male ApoE mice

Project description:In this study we used microarrays to examine relative genes expression within the aorta of ApoE-/- infused with angiotensin II in relation to aneurysm formation. Infusion of angiotensin II induces aortic dilatation particularly of the suprarenal aorta in ApoE-/- mice. Based on studies carried out in our and other laboratories the response to angiotensin II is variable, with some mice developing large aneurysms but other animals appearing resistant to aneurysm formation with aortic diameters similar to that of saline controls. We compared RNA expression from whole aortas of 17 week old male ApoE-/- mice exposed to angiotensin II (1.44 µg/kg/min) for 4 weeks where there was clear evidence of aortic aneurysm formation (n=5) with that of mice failing to develop aneurysms (n=7) and those exposed to saline infusion (n=6). AAA was defined as diameter of suprarenal aorta greated than 1.5mm measured on photographs of aortas at necroscopy. Keywords: Disease state analysis

2009-08-26 | GSE12591 | GEO

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