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a(MESH:"Cell Adhesion Molecules")

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

Name
Cell Adhesion Molecules
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 10

a(CHEBI:"iron(2+)") increases a(MESH:"Cell Adhesion Molecules") 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:"nitric oxide") decreases a(MESH:"Cell Adhesion Molecules") View Subject | View Object

Furthermore, NO has a fundamental role in normal vascular physiology by inhibiting both platelet aggregation and endothelial adhesion molecule expression, as detailed below PubMed:25307023

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

a(CHEBI:heme) positiveCorrelation a(MESH:"Cell Adhesion Molecules") View Subject | View Object

Free heme has been proved possess pro-inflammatory activities, such as leukocyte activation, migration and infiltration, adhesion molecules activation, and cytokines and acute phase proteins induction [17, 18]. PubMed:24464629

Appears in Networks:
Annotations
MeSH
Kidney
Text Location
Introduction

a(CHEBI:heme) increases a(MESH:"Cell Adhesion Molecules") 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

a(CHEBI:heme) positiveCorrelation a(MESH:"Cell Adhesion Molecules") View Subject | View Object

Hemin induces expression of the adhesion molecules on endothelial cells [7, 8] and enables firm neutrophil attachment to the endothelium and initiation of an inflammatory response [9, 10]. PubMed:28716864

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

a(CHEBI:heme) positiveCorrelation a(MESH:"Cell Adhesion Molecules") View Subject | View Object

Based on the previous findings that hemin induces neutrophil adhesion to endothelial cells [8] and that A1AT protects endothelial cells from neutrophil adhesion induced by fMLP [27], we investigated whether A1AT, as a scavenger of hemin, can prevent hemin-induced neutrophil adhesion to HUVECs. As shown in Fig. 4, neutrophils treated with hemin or fMLP (used as a positive control) exhibited a 3-fold higher adhesion to HUVECs compared with controls. However, the adherence of neutrophils treated with hemin/A1AT did not differ from controls (Fig. 4). PubMed:28716864

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

a(MESH:ferrylhemoglobin) increases a(MESH:"Cell Adhesion Molecules") View Subject | View Object

We recently found that, contrary to other forms of oxidized hemoglobin, ferrylhemoglobin acts as a potent pro-inflammatory agonist in endothelial cells, leading to the up-regulation of adhesion molecules that support the recruitment of macrophages into the vessel wall.36 PubMed:20378845

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

p(HGNC:SERPINA1) decreases a(MESH:"Cell Adhesion Molecules") View Subject | View Object

Based on the previous findings that hemin induces neutrophil adhesion to endothelial cells [8] and that A1AT protects endothelial cells from neutrophil adhesion induced by fMLP [27], we investigated whether A1AT, as a scavenger of hemin, can prevent hemin-induced neutrophil adhesion to HUVECs. As shown in Fig. 4, neutrophils treated with hemin or fMLP (used as a positive control) exhibited a 3-fold higher adhesion to HUVECs compared with controls. However, the adherence of neutrophils treated with hemin/A1AT did not differ from controls (Fig. 4). PubMed:28716864

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

p(HGNC:CD40LG) increases a(MESH:"Cell Adhesion Molecules") View Subject | View Object

Furthermore, haem-induced release of P-selectin and VWF is mediated by TLR4 and NFkB signalling. PubMed:25307023

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

p(HGNC:HMOX1) decreases a(MESH:"Cell Adhesion Molecules") View Subject | View Object

During the resolution phase of inflammation HO-1 expression in leukocytes reduces adhesion molecules expression and leukocytes migration, thus contributing to wound healing (Wagener et al., 2003a). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

Out-Edges 4

a(MESH:"Cell Adhesion Molecules") positiveCorrelation a(CHEBI:heme) View Subject | View Object

Free heme has been proved possess pro-inflammatory activities, such as leukocyte activation, migration and infiltration, adhesion molecules activation, and cytokines and acute phase proteins induction [17, 18]. PubMed:24464629

Appears in Networks:
Annotations
MeSH
Kidney
Text Location
Introduction

a(MESH:"Cell Adhesion Molecules") positiveCorrelation a(CHEBI:heme) View Subject | View Object

Hemin induces expression of the adhesion molecules on endothelial cells [7, 8] and enables firm neutrophil attachment to the endothelium and initiation of an inflammatory response [9, 10]. PubMed:28716864

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

a(MESH:"Cell Adhesion Molecules") positiveCorrelation a(CHEBI:heme) View Subject | View Object

Based on the previous findings that hemin induces neutrophil adhesion to endothelial cells [8] and that A1AT protects endothelial cells from neutrophil adhesion induced by fMLP [27], we investigated whether A1AT, as a scavenger of hemin, can prevent hemin-induced neutrophil adhesion to HUVECs. As shown in Fig. 4, neutrophils treated with hemin or fMLP (used as a positive control) exhibited a 3-fold higher adhesion to HUVECs compared with controls. However, the adherence of neutrophils treated with hemin/A1AT did not differ from controls (Fig. 4). PubMed:28716864

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

a(MESH:"Cell Adhesion Molecules") increases path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

Essential for the development of DIC during sepsis is the so-called pro-coagulatory shift of the endothelial cells, caused among others by an increased expression of tissue factor and adhesion molecules especially by damaged endothelial cells [87]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Sepsis
Text Location
Review

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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.