| pubmed-article:9091581 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9091581 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
| pubmed-article:9091581 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:9091581 | lifeskim:mentions | umls-concept:C0115305 | lld:lifeskim |
| pubmed-article:9091581 | lifeskim:mentions | umls-concept:C0134835 | lld:lifeskim |
| pubmed-article:9091581 | lifeskim:mentions | umls-concept:C0700624 | lld:lifeskim |
| pubmed-article:9091581 | lifeskim:mentions | umls-concept:C0004083 | lld:lifeskim |
| pubmed-article:9091581 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:9091581 | pubmed:dateCreated | 1997-4-10 | lld:pubmed |
| pubmed-article:9091581 | pubmed:abstractText | In this study, we examined the relationship between the endothelial selectins (P-selectin and E-selectin) and whether they are critical for alpha4-integrin-dependent leukocyte recruitment in inflamed (late phase response), cremasteric postcapillary venules. Animals were systemically sensitized and 2 wk later challenged intrascrotally with chicken ovalbumin. Leukocyte rolling flux, adhesion, and emigration were assessed at baseline and 4 and 8 h postantigen challenge. There was a significant increase in leukocyte rolling flux, adhesion, and emigration in sensitized and challenged mice at both 4 and 8 h. At 8 h, the increase in leukocyte rolling flux was approximately 50% inhibitable by an anti-alpha4-integrin antibody, 98% inhibitable by fucoidin (a selectin-binding carbohydrate), and 100% inhibitable by an anti-P-selectin antibody. P-selectin-deficient animals displayed no leukocyte rolling or adhesion at 8 h after challenge. However, at 8 h there were many emigrated leukocytes in the perivascular space suggesting P-selectin-independent rolling at an earlier time point. Indeed, at 4 h postantigen challenge in P-selectin-deficient mice, there was increased leukocyte rolling, adhesion, and emigration. The rolling in the P-selectin-deficient mice at 4 h was largely alpha4-integrin dependent. However, there was an essential E-selectin-dependent component inasmuch as an anti-E-selectin antibody completely reversed the rolling, and in E-selectin and P-selectin double deficient mice rolling, adhesion and emigration were completely absent. These results illustrate that P-selectin underlies all of the antigen-induced rolling with a brief transient contribution from E-selectin in the P-selectin-deficient animals. Finally, the antigen-induced alpha4-integrin-mediated leukocyte recruitment is entirely dependent upon endothelial selectins. | lld:pubmed |
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| pubmed-article:9091581 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9091581 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9091581 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9091581 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9091581 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:9091581 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:9091581 | pubmed:author | pubmed-author:SmithC WCW | lld:pubmed |
| pubmed-article:9091581 | pubmed:author | pubmed-author:BeaudetA LAL | lld:pubmed |
| pubmed-article:9091581 | pubmed:author | pubmed-author:KanwarSS | lld:pubmed |
| pubmed-article:9091581 | pubmed:author | pubmed-author:WolitzkyB ABA | lld:pubmed |
| pubmed-article:9091581 | pubmed:author | pubmed-author:KubesPP | lld:pubmed |
| pubmed-article:9091581 | pubmed:author | pubmed-author:HickeyM JMJ | lld:pubmed |
| pubmed-article:9091581 | pubmed:author | pubmed-author:BullardD CDC | lld:pubmed |
| pubmed-article:9091581 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9091581 | pubmed:day | 17 | lld:pubmed |
| pubmed-article:9091581 | pubmed:volume | 185 | lld:pubmed |
| pubmed-article:9091581 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9091581 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9091581 | pubmed:pagination | 1077-87 | lld:pubmed |
| pubmed-article:9091581 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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