Neutrophil Proteinase 3 Acts on Protease-Activated Receptor-2 to Enhance Vascular Endothelial Cell Barrier Function
Author(s) -
Christopher J. Kuckleburg,
Peter J. Newman
Publication year - 2012
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.112.300474
Subject(s) - microbiology and biotechnology , endothelial stem cell , endothelial protein c receptor , protease activated receptor , endothelium , vascular permeability , barrier function , receptor , proteases , serine protease , biology , protease , thrombin , immunology , in vitro , biochemistry , platelet , enzyme , endocrinology
The principle role of the vascular endothelium is to present a semi-impermeable barrier to soluble factors and circulating cells, while still permitting the passage of leukocytes from the bloodstream into the tissue. The process of diapedesis involves the selective disruption of endothelial cell junctions, which could compromise vascular integrity. It is therefore somewhat surprising that neutrophil transmigration does not significantly impair endothelial barrier function. We examined whether neutrophils might secrete factors that promote vascular integrity during the latter stages of neutrophil transmigration, in particular, the role of neutrophil serine proteinase 3 (PR3).
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