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Role of neutrophils and β2 integrins in platelet extravasation in corneal limbal venules following epithelial wound injury (671.10)
Author(s) -
Li Zhijie,
Smith C,
Gagen Debjani,
Lam Fong,
Burns Alan,
Rumbaut Rolando
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.671.10
Subject(s) - extravasation , platelet , integrin , medicine , leukocyte extravasation , immunology , cd18 , p selectin , pathology , platelet activation , wound healing , antibody , inflammation , receptor , monoclonal antibody
Corneal epithelial wound injury in the mouse results in an acute inflammatory response in the surrounding peripheral limbal microvessels. We showed previously that in wild‐type mice neutrophils (PMNs) and platelets accumulate at the inflamed limbus in a co‐dependent manner and approximately 50% of platelets are evident in the extravascular space; the mechanisms by which platelets extravasate are unclear. To determine the role of PMNs and β2 integrins on platelet extravasation, we quantified platelet recruitment in corneal vessels in mice after antibody‐induced depletion of neutrophils (anti‐Ly6G); control mice received isotype control antibody. We also compared extravascular platelet numbers in wild‐type mice and mice deficient in CD18. Anti‐Ly6G antibodies decreased total platelet numbers in corneal limbal vessels 24 hours after epithelial injury (from 141 ± 15 to 66 ± 16 platelets per field, p<0.05) and reduced the relative proportion of extravascular platelets (from 56 ± 5 % to 9 ± 1%, p< 0.001). Similarly, mice deficient in CD18 had a substantial decrease in extravascular platelets following corneal injury. Platelet‐PMN contact was evident in the intravascular and extravascular space by immunofluorescence and electron microscopy. These studies demonstrate that PMNs and β2 integrins contribute to platelet extravasation from corneal limbal vessels following epithelial wound injury. Grant Funding Source : Supported by R01 HL‐ 116524, and a Merit Review Grant from The Department of Veterans Affairs