Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Copper regulation of HIF-1 transcriptional activities

ABSTRACT: HIF-1 regulated VEGF expression were upregulated in reponse to ischemic injury. However, the VEGF mRNA level were increased in the early stage but decreased in the late stage of myocardial infarction. We found that activities of HIF-1 binding to the HRE sites were possiblely responsible for the differential expression of VEGF. The HIF-1 binding activities were regulated by copper. After ischemic injury, copper concentrations were decreased in the infarct myocardium in the late stage of myocardial infarction, which might reduce VEGF expression through insufficient HIF-1 binding to HRE sites.

ORGANISM(S): Macaca mulatta

PROVIDER: GSE125755 | GEO | 2022/01/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Bone marrow adipocytes fuel emergency hematopoiesis

Project description:Hematopoiesis advances cardiovascular disease by generating inflammatory leukocytes that attack the arteries, heart and brain. While it is well documented that the bone marrow niche regulates hematopoietic stem cell proliferation and hence the systemic leukocyte pool, it is less clear how cardiovascular disease affects the vasculature forming this niche. Here we show that arterial hypertension, atherosclerosis and myocardial infarction alter the anatomy and function of bone marrow vasculature. Hypertension and atherosclerosis instigated vascular fibrosis, leakage and endothelial dysfunction in the bone marrow. Myocardial infarction induced vascular leakage and bone marrow angiogenesis via Vegf signaling. Endothelial cell-specific deletion of the Vegf receptor 2 limited emergency hematopoiesis after myocardial infarction, indicating that new vasculature supports higher blood cell production. RNA-sequencing of bone marrow endothelial cells revealed inflammatory gene expression in mice with cardiovascular disease. Endothelial cell-specific deletion of interleukin 6 or versican, which were highly expressed in mice with atherosclerosis or myocardial infarction, respectively, reduced hematopoiesis and systemic myeloid cells. Taken together, cardiovascular disease affects the vascular bone marrow niche, thus influencing hematopoietic stem cell behavior and expanding innate immune cell supply to atherosclerotic plaque and ischemic myocardium. Interrupting this feed back loop may constrain cardiovascular inflammation.

2023-11-04 | GSE169267 | GEO

Cardiovascular disease perturbs the vascular hematopoietic stem cell niche

2021-09-27 | GSE144498 | GEO

Targeting Immune-Fibroblast Crosstalk in Myocardial Infarction and Cardiac Fibrosis I

Project description:To define the cellular landscape of human myocardial infarction and heart failure, we performed Cellular Indexing of Transcriptomes and Epitomes by sequencing (CITE-seq) in 22 explanted human hearts from healthy donors, acute myocardial infarction (MI),and chronic ischemic and non-ischemic cardiomyopathy patients.

2024-07-01 | GSE217494 | GEO

Transcription profiling of human left ventricular apex samples

Project description:19 paired human left ventricular apex samples were harvested at the time of implant of a left ventricular assist device (PRE) and at the time of explant (POST). The cohort included patients that were clinically classified as ischemic (I) showing evidence of coronary artery disease, non-ischemic (N) no evidence of coronary artery disease or acute Myocardial infarction (IM) myocardial infarction within 10 days of the implant. Tissue was processed and hybridized to the Affymetrix HG-U133A chip.

2007-10-02 | E-GEOD-974 | biostudies-arrayexpress

Effects of Post-Myocardial Infarction Heart Failure on the Bone Vascular Niche (Mouse Data)

Project description:We demonstrate an age-independent loss of type H bone endothelium in heart failure after myocardial infarction in both mice and in humans. Using single-cell RNA sequencing, we delineate the transcriptional heterogeneity of human bone marrow endothelium showing increased expression of inflammatory genes, including IL1B and MYC, in ischemic heart failure. Endothelial-specific overexpression of MYC was sufficient to induce type H bone endothelial cells, whereas inhibition of NLRP3-dependent IL-1 production partially prevents the post-myocardial infarction loss of type H vasculature in mice.

2021-05-13 | E-MTAB-10448 | biostudies-arrayexpress

Effects of Post-Myocardial Infarction Heart Failure on the Bone Vascular Niche (Human Data)

2021-05-11 | E-MTAB-10432 | biostudies-arrayexpress

Left ventricular apex samples

Project description:19 paired human left ventricular apex samples were harvested at the time of implant of a left ventricular assist device (PRE) and at the time of explant (POST). The cohort included patients that were clinically classified as "ischemic" (I) showing evidence of coronary artery disease, "non-ischemic" (N) no evidence of coronary artery disease or "acute Myocardial infarction" (IM) myocardial infarction within 10 days of the implant. Tissue was processed and hybridized to the Affymetrix HG-U133A chip. Keywords: other

2004-01-18 | GSE974 | GEO

Copper regulation of HIF-1 transcriptional activities

Project description:Copper regulation of HIF-1 transcriptional activities

| PRJNA517453 | ENA

Hypoxia inducible factors individually facilitate inflammatory myeloid metabolism and inefficient cardiac repair

Project description:Following myocardial infarction, tissue ischemia leads to activation of hypoxia inducible factors. DeBerge et al. demonstrate that HIF-1a and HIF-2a activation in myeloid cells antagonizes cardiac repair pathways through cleavage of cardioprotective MerTK and suppression of anti-inflammatory mitochondrial metabolism, respectively.

2021-07-24 | GSE180678 | GEO

Post Acute Myocardial Infarction Left Ventricular Remodeling Bio marker Analysis (PAMILA)

Project description:Patients with acute myocardial infarction (a condition classified under coronary heart disease, including STEMI and NSTEMI) are at high risk for recurrent ischemic events, but the pathways and factors which contribute to this elevated risk are incompletely understood. This study aims to identify biomarkers associated with acute myocardial infarction through various omics strategies. For the identified biomarkers, we aim to demonstrate prognostic value, and predict/stratify the risks of adverse cardiovascular events (e.g., stroke, heart failure, death).

2021-08-15 | ST001908 | MetabolomicsWorkbench

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