Source:http://linkedlifedata.com/resource/pubmed/id/20716766
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
22
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pubmed:dateCreated |
2010-11-26
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pubmed:abstractText |
von Willebrand factor (VWF) is an important player in hemostasis but has also been suggested to promote inflammatory processes. Gene ablation of VWF causes a simultaneous defect in P-selectin expression making it difficult to identify VWF-specific functions. Therefore, we analyzed whether blocking antibodies against VWF would be able to interfere with neutrophil extravasation. We found that these antibodies inhibited neutrophil recruitment into thioglycollate-inflamed peritoneum and KC-stimulated cremaster by approximately 50%. Whereas platelet-VWF was not involved, the contribution of VWF to granulocyte recruitment was strictly dependent on the presence of platelets and the accessibility of their VWF-receptor glycoprotein Ib. Surprisingly, platelet P-selectin was largely dispensable for leukocyte extravasation, in agreement with our observation that anti-VWF antibodies did not affect leukocyte rolling and adhesion. Searching for possible effects downstream of leukocyte capture, we found that anti-VWF antibodies significantly inhibited thioglycollate-induced vascular permeability. The increase of permeability was independent of circulating granulocytes, showing that it was not a side effect of neutrophil diapedesis. Collectively, our results demonstrate that VWF-associated platelets strongly support neutrophil extravasation at a step downstream of leukocyte docking to the vessel wall. This step could be related to leukocyte diapedesis facilitated by destabilization of the endothelial barrier.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1528-0020
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pubmed:author |
pubmed-author:BroermannAndreA,
pubmed-author:GoergeTobiasT,
pubmed-author:JonesClaireC,
pubmed-author:KhandogaAlexander GAG,
pubmed-author:KrombachFritzF,
pubmed-author:LiHangH,
pubmed-author:NieswandtBernhardB,
pubmed-author:PetriBjörnB,
pubmed-author:SchneiderStefan WSW,
pubmed-author:VestweberDietmarD,
pubmed-author:WildMartin KMK,
pubmed-author:ZarbockAlexanderA
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pubmed:issnType |
Electronic
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pubmed:day |
25
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pubmed:volume |
116
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4712-9
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pubmed:meshHeading |
pubmed-meshheading:20716766-Animals,
pubmed-meshheading:20716766-Antibodies,
pubmed-meshheading:20716766-Blood Platelets,
pubmed-meshheading:20716766-Capillary Permeability,
pubmed-meshheading:20716766-Cell Movement,
pubmed-meshheading:20716766-Leukocytes,
pubmed-meshheading:20716766-Mice,
pubmed-meshheading:20716766-Mice, Inbred C57BL,
pubmed-meshheading:20716766-Neutrophils,
pubmed-meshheading:20716766-P-Selectin,
pubmed-meshheading:20716766-Peritoneum,
pubmed-meshheading:20716766-Peritonitis,
pubmed-meshheading:20716766-Platelet Glycoprotein GPIb-IX Complex,
pubmed-meshheading:20716766-von Willebrand Factor
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pubmed:year |
2010
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pubmed:articleTitle |
von Willebrand factor promotes leukocyte extravasation.
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pubmed:affiliation |
Max Planck Institute for Molecular Biomedicine, Münster, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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