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bp(GO:vasoconstriction)

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Entity

Name
vasoconstriction
Namespace
go
Namespace Version
20180921
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

Appears in Networks 1

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 8

a(CHEBI:"nitric oxide") increases bp(GO:vasoconstriction) View Subject | View Object

The extensive crosslinkage of cell-free hemoglobin in a high-molecular weight HBOC retains cell-free hemoglobin dimers in the intravascular compartment, thereby preventing extravasation 112 of cell-free hemoglobin into the muscular layer of the arteries where local NO consumption can trigger vasoconstriction (25). PubMed:28314763

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a(CHEBI:"nitric oxide") negativeCorrelation bp(GO:vasoconstriction) View Subject | View Object

Heme promotes endothelial dysfunction by inducing the expression of adhesion molecules and reducing nitric oxide (NO) availability, which causes vasoconstriction [9-14]. PubMed:28400318

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Cell Ontology (CL)
endothelial cell
Text Location
Introduction

a(CHEBI:heme) increases bp(GO:vasoconstriction) View Subject | View Object

Cell-free hemoglobin and its prosthetic group heme can contribute to organ dysfunction and death [1–4, 9–12]; the pathological mechanisms include nitric oxide consumption, vasoconstriction, oxidative injury to lipid membranes, activation of the transcription factor NF-κB, endothelial injury as well as iron-driven oxidative inhibition of glucose metabolism[10–14]. PubMed:29956069

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Review

p(HGNC:HBB) increases bp(GO:vasoconstriction) View Subject | View Object

Several studies in animals have supported the idea that infusion of free Hb, stored RBC supernatant (preservation solution + plasma), and Hb-containing microvesicles causes vasoconstriction, vascular dysfunction, and vascular injury.12,16–18 PubMed:27308950

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MeSH
Arteries
Text Location
Introduction

p(HGNC:HBB) positiveCorrelation bp(GO:vasoconstriction) View Subject | View Object

Plasma hemoglobin scavenges nitric oxide and causes vasoconstriction, platelet aggregation and inflammation9,22–24. PubMed:27515135

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p(HGNC:HBB) increases bp(GO:vasoconstriction) View Subject | View Object

Previous studies showed that db/db mice have enhanced 312 susceptibility to hemoglobin-induced vasoconstriction (25). PubMed:28314763

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MeSH
Diabetes Mellitus
Text Location
Introduction

p(MGI:Hp) decreases bp(GO:vasoconstriction) View Subject | View Object

Schaer and colleagues 107 showed that administration of exogenous haptoglobin prevents extravasation of cell free hemoglobin and vasoconstriction in rats (18). PubMed:28314763

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path(MESH:Hemolysis) positiveCorrelation bp(GO:vasoconstriction) View Subject | View Object

Thus, haemolysis results in NO scavenging, systemic vasoconstriction and increased blood stasis, thereby affecting one of the principle components of Virchow’s Triad. PubMed:25307023

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Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

Out-Edges 3

bp(GO:vasoconstriction) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Thus, haemolysis results in NO scavenging, systemic vasoconstriction and increased blood stasis, thereby affecting one of the principle components of Virchow’s Triad. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

bp(GO:vasoconstriction) positiveCorrelation p(HGNC:HBB) View Subject | View Object

Plasma hemoglobin scavenges nitric oxide and causes vasoconstriction, platelet aggregation and inflammation9,22–24. PubMed:27515135

Appears in Networks:
Annotations
Text Location
Introduction

bp(GO:vasoconstriction) negativeCorrelation a(CHEBI:"nitric oxide") View Subject | View Object

Heme promotes endothelial dysfunction by inducing the expression of adhesion molecules and reducing nitric oxide (NO) availability, which causes vasoconstriction [9-14]. PubMed:28400318

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
Text Location
Introduction

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.