Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

JAK2V617F-dependent clonal hematopoiesis drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm

ABSTRACT: JAK2V617F-dependent clonal hematopoiesis drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm

PROVIDER: PRJNA890296 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21896000_1.fastq.gz	Fastqsanger.gz
	SRR21896000_2.fastq.gz	Fastqsanger.gz
	SRR21896001_1.fastq.gz	Fastqsanger.gz
	SRR21896001_2.fastq.gz	Fastqsanger.gz
	SRR21896002_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 80

Similar Datasets

JAK2V617F-dependent clonal hematopoiesis drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm

Project description:In order to understand the mechanisms responsible for lethal JAK2V617F-dependent aortic disease, we performed RNA sequencing in the aorta of 7-week old Jak2V617F HC-EC and control Jak2WT mice

2022-10-20 | GSE215455 | GEO

scRNA-seq/CITE-seq analysis of aortic CD45+ cells from mice expressing Jak2V617F mutation in myeloid cells

Project description:JAK2V617F mutation is associated with an increased risk for athero-thrombotic cardiovascular disease, but its role in aortic disease development and complications remains unknown. In a cohort of patients with myeloproliferative neoplasm, JAK2V617F mutation was identified as an independent risk factor for dilation of both the ascending and descending thoracic aorta. Using single-cell RNA-seq, complementary genetically-modified mouse models, as well as pharmacological approaches, we found that JAK2V617F mutation was associated with a pathogenic pro-inflammatory phenotype of perivascular tissue-resident macrophages, which promoted deleterious aortic wall remodeling at early stages, and dissecting aneurysm through the recruitment of circulating monocytes at later stages. Finally, genetic manipulation of tissue-resident macrophages, or treatment with a Jak2 inhibitor, ruxolitinib, mitigated aortic wall inflammation and reduced aortic dilation and rupture. Overall, JAK2V617F mutation drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm.

2022-10-26 | GSE214880 | GEO

JAK2V617F mutation drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm.

| S-EPMC9633755 | biostudies-literature

Dissecting aortic aneurysm in Marfan syndrome is associated with losartan-sensitive transcriptomic modulation of aortic cells

Project description:To improve our limited understanding of the pathogenesis of thoracic aortic aneurysm (TAA) leading to acute aortic dissection, we used single-cell RNA sequencing to profile disease-relevant transcriptomic changes of aortic cell populations in a well-characterized mouse model of the most commonly diagnosed form of Marfan syndrome (MFS). As result,MFSmod were identified only in the aorta of Fbn1mgR/mgR mice. In situ hybridizations of diagnostic transcripts located MFSmod cells to the intima of Fbn1mgR/mgR aortas. Consistent with angiotensin II type I receptor (At1r) contribution to TAA development, MFSmod cells were absent in the aorta of Fbn1mgR/mgR mice treated with the At1r antagonist losartan. Altogether, our findings indicate that a discrete dynamic alteration of aortic cell identity is associated with dissecting TAA in MFS mice and increased risk of aortic dissection in MFS patients.

2023-06-27 | GSE227776 | GEO

Aortic Aneurysm iTRAQ HiRIEF proteomics

Project description:Conducted proteomics on samples from patients with aortic aneurysm and from non-dilated controls. Furthermore, we investigated both patients with bicuspid aortic valves (BAV) and also the more normal tricuspid aortic valves (TAV). The aim was to elucidate the molecular mechanisms behind the higher propensity of BAV patients to develop aorta dilation and consequent aortic aneurysm.

2017-03-31 | MSV000080837 | MassIVE

Aortic Aneurysm iTRAQ HiRIEF proteomics

2016-12-23 | PXD003702 | Pride

Dissecting aortic aneurysm in Marfan syndrome is associated with losartan-sensitive transcriptomic modulation of aortic cells

Project description:Dissecting aortic aneurysm in Marfan syndrome is associated with losartan-sensitive transcriptomic modulation of aortic cells

| PRJNA946797 | ENA

Identification of novel biomarkers for aortic aneurysm

Project description:To discover novel biomarkers for aortic aneurysm, serum samples of patients with thoracic aortic aneurysm were fractionated, tryptic digested, and subjected to proteome analysis.

2023-11-15 | PXD033774 | JPOST Repository

Expression data from control, aortic aneurysm, and aortic dissection cells

Project description:Aneurysmatic and dissection cells show a specific alteration of gene expression, which allow a disease specific distinction. We used microarrays to analyse the cellular gene expression of controls, thoracic aortic aneurysm, and aortic dissection.

2022-12-02 | GSE219204 | GEO

IL-27 receptor signaling regulated stress hematopoiesis drives Abdominal Aortic Aneurysm development

Project description:Abdominal Aortic Aneurysm (AAA) is a prevalent life-threatening disease, where aortic wall degradation is mediated by accumulated immune cells. Though cytokines regulate inflammation within the aorta, their contribution to AAA via distant alterations, particularly in the control of hematopoietic stem cell (HSC) differentiation remains poorly defined. Here we report a pathogenic role for the interleukin-27 receptor (IL-27R) in AAA as genetic ablation of IL-27R protects mice from the disease development, where the mitigation of AAA is associated with a blunted accumulation of myeloid cells in the aorta due to the attenuation of Ang II-induced HSC expansion. The loss of IL-27R engages transcriptional programs that promote HSCs quiescence and suppresses differentiation decreasing mature myeloid cell production and accumulation in the aorta. Our studies illuminate how a prominent vascular disease can be distantly driven by cytokine dependent regulation of bone marrow precursors.

2019-10-14 | GSE129881 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data