pubmed-article:11827998 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11827998 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:11827998 | lifeskim:mentions | umls-concept:C0014072 | lld:lifeskim |
pubmed-article:11827998 | lifeskim:mentions | umls-concept:C1843571 | lld:lifeskim |
pubmed-article:11827998 | lifeskim:mentions | umls-concept:C1850419 | lld:lifeskim |
pubmed-article:11827998 | lifeskim:mentions | umls-concept:C1970036 | lld:lifeskim |
pubmed-article:11827998 | lifeskim:mentions | umls-concept:C0162337 | lld:lifeskim |
pubmed-article:11827998 | lifeskim:mentions | umls-concept:C0205349 | lld:lifeskim |
pubmed-article:11827998 | lifeskim:mentions | umls-concept:C0332162 | lld:lifeskim |
pubmed-article:11827998 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:11827998 | pubmed:dateCreated | 2002-2-5 | lld:pubmed |
pubmed-article:11827998 | pubmed:abstractText | Platelet/endothelial cell adhesion molecule-1 (PECAM-1, CD31), a 130-kDa glycoprotein member of the Ig superfamily of transmembrane proteins, is expressed on endothelial cells, platelets, and subsets of leukocytes. It functions as a cell adhesion molecule as well as a scaffolding molecule capable of modulating cellular signaling pathways. In this study, using PECAM-1-deficient (KO) mice, as well as cells derived from these mice, we demonstrate that the absence of PECAM-1 expression is associated with an early onset of clinical symptoms during experimental autoimmune encephalomyelitis (EAE), a mouse model for the human autoimmune disease multiple sclerosis. During EAE, mononuclear cell extravasation and infiltration of the CNS occur at earlier time points in PECAM-KO mice than in wild-type mice. In vitro, T lymphocyte transendothelial migration across PECAM-KO endothelial cells is enhanced, regardless of expression of PECAM-1 on transmigrating T cells. Additionally, cultured PECAM-KO endothelial cells exhibit prolonged permeability changes in response to histamine treatment compared with PECAM-1-reconstituted endothelial cells. Lastly, we demonstrate an exaggerated and prolonged CNS vascular permeability during the development of EAE and a delay in restoration of dermal vascular integrity following histamine challenge in PECAM-KO mice. | lld:pubmed |
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pubmed-article:11827998 | pubmed:language | eng | lld:pubmed |
pubmed-article:11827998 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11827998 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:11827998 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11827998 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11827998 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11827998 | pubmed:month | Feb | lld:pubmed |
pubmed-article:11827998 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:11827998 | pubmed:author | pubmed-author:MadriJoseph... | lld:pubmed |
pubmed-article:11827998 | pubmed:author | pubmed-author:GraesserDonna... | lld:pubmed |
pubmed-article:11827998 | pubmed:author | pubmed-author:SolowiejAnnaA | lld:pubmed |
pubmed-article:11827998 | pubmed:author | pubmed-author:BrucknerMonik... | lld:pubmed |
pubmed-article:11827998 | pubmed:author | pubmed-author:OsterweilEmil... | lld:pubmed |
pubmed-article:11827998 | pubmed:author | pubmed-author:JuedesAmyA | lld:pubmed |
pubmed-article:11827998 | pubmed:author | pubmed-author:DavisSandraS | lld:pubmed |
pubmed-article:11827998 | pubmed:author | pubmed-author:RuddleNancy... | lld:pubmed |
pubmed-article:11827998 | pubmed:author | pubmed-author:EngelhardtBri... | lld:pubmed |
pubmed-article:11827998 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11827998 | pubmed:volume | 109 | lld:pubmed |
pubmed-article:11827998 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11827998 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11827998 | pubmed:pagination | 383-92 | lld:pubmed |
pubmed-article:11827998 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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