Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Enzyme
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Query: UMLS:C0031154 (
peritonitis
)
15,372
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The third member of the family of junctional adhesion molecules (JAMs),
JAM-3
, also called
JAM-C
, was recently shown to be a novel counter-receptor on platelets for the leukocyte beta(2)-integrin Mac-1 (alphaMbeta(2), CD11b/CD18). Here, new functional aspects of the role of endothelial cell
JAM-C
were investigated. Endothelial cells express
JAM-C
, which is predominantly localized within junctions at interendothelial contacts, since it codistributes with a tight junction component, zonula occludens-1. Whereas
JAM-C
does not participate in neutrophil adhesion to endothelial cells, it mediates neutrophil transmigration in a Mac-1-dependent manner. In particular, inhibition of
JAM-C
significantly reduced neutrophil transendothelial migration, and the combination of
JAM-C
and platelet/endothelial cell adhesion molecule-1 blockade almost completely abolished neutrophil transendothelial migration in vitro. In vivo, inhibition of
JAM-C
with soluble mouse
JAM-C
resulted in a 50% reduction of neutrophil emigration in the mouse model of acute thioglycollate-induced
peritonitis
. Thus,
JAM-C
participates in neutrophil transmigration and thereby provides a novel molecular target for antagonizing interactions between vascular cells that promote inflammatory vascular pathologies.
...
PMID:The junctional adhesion molecule-C promotes neutrophil transendothelial migration in vitro and in vivo. 1548 32
