Differential Expression of E- and P-Selectin in the Microvasculature of Sickle Cell Transgenic Mice

Objective:There is a growing body of evidence that endothelial cells assume an inflammatory phenotype in sickle cell disease. The authors determined whether (1) the expression of E- and P-selectin differs between sickle cell transgenic (βS) mice and their wild-type counterparts, and (2) blood platel...

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Published in:Microcirculation (New York, N.Y. 1994) Vol. 11; no. 4; pp. 377 - 385
Main Authors: Wood, Katherine, Russell, Janice, Hebbel, Robert P., Grange, D. Neil
Format: Journal Article
Language:English
Published: Oxford, UK Informa UK Ltd 01-06-2004
Blackwell Publishing Ltd
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Summary:Objective:There is a growing body of evidence that endothelial cells assume an inflammatory phenotype in sickle cell disease. The authors determined whether (1) the expression of E- and P-selectin differs between sickle cell transgenic (βS) mice and their wild-type counterparts, and (2) blood platelets and/or neutrophils contribute to the altered selectin expression. Methods:Expression of E- and P-selectin was measured in different regional vascular beds of wild-type and βSmice (with or without thrombocytopenia or neutropenia) using the dual radiolabeled monoclonal antibody technique. Results:Constitutive expression of P-selectin was significantly increased in the heart, lungs, small bowel, large bowel, and penis of βSversus WT mice. While thrombocytopenia reduced P-selectin expression in the small bowel and penis of βSmice, neutropenia was associated with a reduction in P-selectin expression only in the penis. E-selectin expression was not significantly elevated in any vascular bed except the penis of βSmice. Conclusions:Sickle cell disease promotes an increased P-selectin expression in several vascular beds. An accumulation of platelets may explain the increased P-selectin expression observed in some vascular beds. Microcirculation(2004) 11,377-385. doi:10.1080/10739680490437559
Bibliography:ark:/67375/WNG-L1XFHG6V-M
istex:325A246C30CEE029B3667A32132DE5A60BD446C9
ArticleID:MICC407
Supported by grants from the National Institutes of Health (DK43785 and P01‐HL55552).
ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:1073-9688
1549-8719
DOI:10.1080/10739680490437559