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

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

PROVIDER: PRJNA1173561 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31014722_1.fastq.gz	Fastqsanger.gz
	SRR31014722_2.fastq.gz	Fastqsanger.gz
	SRR31014723_1.fastq.gz	Fastqsanger.gz
	SRR31014723_2.fastq.gz	Fastqsanger.gz
	SRR31014724_1.fastq.gz	Fastqsanger.gz

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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

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

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Transcription profiling of ray aortic tissue from different hypertensive models

Project description:To determine if there exists a consistent gene signature associated with vascular hypertrophy among different rat hypertensive models: treated and untreated Wistar Kyoto (WKY) rats and treated and untreated Spontaneous Hypertensive Rat (SHR) rats. Experiment Overall Design: Two strains of rat were studies: WKY which are normotensive and SHR which are hypertensive. Aortic tissue was taken from 6 untreated WKY rats and 6 WKY rats treated with angiotensin. Aortic tissue was taken from 6 untreated SHR rats, 6 treated with nifedipine for two weeks and 5 treated with nifedipine for two weeks and then washed out for three weeks. There was a total of 29 samples. A pool of RNA from 6 untreated WKY rats was used as a reference. Hybridizations were performed in duplicate with a dye-flip and always with the reference as the second color.

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Cardiac Hypertensive-Cmpd17b (therapeutic) - Cell treatment proteomics

Project description:Formyl peptide receptors (FPR) play a critical role in the regulation of resolution of inflammation, an important mediator of hypertension-induced cardiac damage. We have previously discovered an FPR small-molecule prototype Cmpd17b exhibit cardioprotective effects against acute and severe cardiac inflammatory insults, but its impact on chronic cardiac inflammatory insult, such as hypertension, has not been explored. To investigate the therapeutic potential of our FPR agonist on mean arterial pressure (MAP), cardiac remodelling and function in hypertensive mice. This dataset relates to cardiac fibroblasts (human) and smooth muscle aortic cells (SMAC) cell proteome remodelling following Ang-II and Cmp17b treatment

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

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

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Excessive leukotriene B4 in nucleus tractus solitarii is pro-hypertensive in spontaneously hypertensive rats.

Project description:We have used Affymetrix microarray-driven gene profiling to comprehensively describe the expression of mRNAs in the nucleus tractus solitarii (NTS) in the adult male spontaneously hypertensive rat (SHR) as compared to its normotensive parental Wistar-Kyoto (WKY) strain. Keywords: Gene expression NTS was dissected from hypertensive (SHR) and normotensive (WKY) strains of rat. For each structure, 10 independent Affymetrix Genechip 230 2.0 experiments were performed (5 SHR, 5 WKY), with each chip representing an independent biological replication (n=5).

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

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Excessive leukotriene B4 in nucleus tractus solitarii is pro-hypertensive in spontaneously hypertensive rats.

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Single-Cell RNA-Seq Reveals Adventitial Fibroblast Alterations during Mouse Atherosclerosis

Project description:Background: Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of mortality in the western world despite the success of lipid lowering therapies, highlighting the need for novel lipid-independent therapeutic strategies. Genome-wide association studies (GWAS) have identified numerous genes associated with ASCVD that appear to predominantly function in the vessel wall, suggesting both that vascular cells mediate ASCVD, and that the genes and pathways essential for this vascular cell function may be novel therapeutic targets for the treatment of ASCVD. Furthermore, some of these implicated genes appear to function in the adventitial layer of the vasculature, suggesting these cells are able to potentiate ASCVD. Methods: To investigate the contribution of adventitial cells in atherosclerosis, we conducted single-cell RNA sequencing (scRNA-seq) of the aortic adventitia during atherogenesis in male Ldlr-/- mice via pools of three mice, two samples per condition. We cross-referenced the scRNA-seq data with human ASCVD GWAS to identify regulators of adventitial responses in ASCVD. These regulators were then validated in vitro in human adventitial fibroblasts. Results: We identified four adventitial fibroblast populations, all of which displayed shifts in population size and gene expression over the course of atherogenesis. SERPINH1, an ASCVD-linked GWAS gene, was differentially expressed in adventitial fibroblasts during atherogenesis. Knockdown of SERPINH1 in vitro reduced fibroblast migration and altered subcluster marker gene expression. Conclusions: These findings reveal dynamic changes in adventitial fibroblasts during atherosclerosis and suggest that reduced SERPINH1 expression disrupts adventitial fibroblast function, contributing to ASCVD progression.

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