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bp(MESH:"Cytotoxicity, Immunologic")

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Entity

Name
Cytotoxicity, Immunologic
Namespace
MeSH
Namespace Version
20181007
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/01c9daa61012b37dd0a1bc962521ba51a15b38f1/external/mesh-names.belns

Appears in Networks 1

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 6

a(CHEBI:"iron(2+)") positiveCorrelation bp(MESH:"Cytotoxicity, Immunologic") View Subject | View Object

Thus, by participating in Fenton chemistry, non-transferrin-bound iron (i.e., iron not bound to the physiological iron transport protein, transferrin) causes oxidative damage, cytotoxicity and enhanced endothelial expression of adhesion molecules, thereby enhancing thrombotic risk (Hershko, 2007). PubMed:25307023

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

a(CHEBI:"oxidised LDL") positiveCorrelation bp(MESH:"Cytotoxicity, Immunologic") View Subject | View Object

Heme/iron-mediated oxidative modification of LDL can cause endothelial cytotoxicity8,24 and – at sublethal doses – the expression of stress-response genes.9,11-14 PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plaque, Atherosclerotic
Text Location
Results

a(HM:"Atheroma lipid") increases bp(MESH:"Cytotoxicity, Immunologic") View Subject | View Object

We have found that atheroma lipids when oxidized by heme are highly cytotoxic to human endothelial cells, and hemopexin reduced this cytotoxicity. PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Atherosclerosis
Text Location
Discussion

a(MESH:"Glutathione Peroxidase") decreases bp(MESH:"Cytotoxicity, Immunologic") View Subject | View Object

Pre-treatment of heme-oxidized lipids with glutathione/glutathione peroxidase reduced the lipid hydroperoxide content (113±30 vs. 74±22 nmol LOOH/mg extract, p<0.01) and inhibited the endothelial cell cytotoxicity by 25% (p<0.05). PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plaque, Atherosclerotic
Text Location
Results

a(MESH:"Reactive Oxygen Species") increases bp(MESH:"Cytotoxicity, Immunologic") View Subject | View Object

These ROS then oxidize cell membrane constituents to induce cytotoxicity and promote inflammation and thrombosis. PubMed:25307023

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

bp(MESH:"Lipid Peroxidation") positiveCorrelation bp(MESH:"Cytotoxicity, Immunologic") View Subject | View Object

Inhibition of lipid oxidation by either haptoglobin or hemopexin reduced the cytotoxicity (Fig 4B) and HO-1 induction caused by sublethal amounts of pretreated atheromatous lesion lipids (Fig 4C and D). PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plaque, Atherosclerotic
Text Location
Results

Out-Edges 3

bp(MESH:"Cytotoxicity, Immunologic") positiveCorrelation a(CHEBI:"oxidised LDL") View Subject | View Object

Heme/iron-mediated oxidative modification of LDL can cause endothelial cytotoxicity8,24 and – at sublethal doses – the expression of stress-response genes.9,11-14 PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plaque, Atherosclerotic
Text Location
Results

bp(MESH:"Cytotoxicity, Immunologic") positiveCorrelation bp(MESH:"Lipid Peroxidation") View Subject | View Object

Inhibition of lipid oxidation by either haptoglobin or hemopexin reduced the cytotoxicity (Fig 4B) and HO-1 induction caused by sublethal amounts of pretreated atheromatous lesion lipids (Fig 4C and D). PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plaque, Atherosclerotic
Text Location
Results

bp(MESH:"Cytotoxicity, Immunologic") positiveCorrelation a(CHEBI:"iron(2+)") View Subject | View Object

Thus, by participating in Fenton chemistry, non-transferrin-bound iron (i.e., iron not bound to the physiological iron transport protein, transferrin) causes oxidative damage, cytotoxicity and enhanced endothelial expression of adhesion molecules, thereby enhancing thrombotic risk (Hershko, 2007). PubMed:25307023

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

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.