pubmed-article:11466334 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11466334 | lifeskim:mentions | umls-concept:C0224522 | lld:lifeskim |
pubmed-article:11466334 | lifeskim:mentions | umls-concept:C1332712 | lld:lifeskim |
pubmed-article:11466334 | lifeskim:mentions | umls-concept:C0041904 | lld:lifeskim |
pubmed-article:11466334 | lifeskim:mentions | umls-concept:C1539477 | lld:lifeskim |
pubmed-article:11466334 | lifeskim:mentions | umls-concept:C0162493 | lld:lifeskim |
pubmed-article:11466334 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
pubmed-article:11466334 | lifeskim:mentions | umls-concept:C0205463 | lld:lifeskim |
pubmed-article:11466334 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:11466334 | pubmed:dateCreated | 2001-7-23 | lld:pubmed |
pubmed-article:11466334 | pubmed:abstractText | CD44 is a ubiquitous molecule known as a hyaluronan receptor. However, the relevance of CD44 to inflammatory processes, for example, rheumatoid synovitis, remains unclear. In this study, we propose a novel function for CD44 using synovial cells from rheumatoid arthritis (RA) patients and demonstrated that CD44 cross-linking augmented Fas expression and subsequent Fas-mediated apoptosis of the cells: 1) cross-linking of CD44 on RA synovial cells markedly augmented Fas expression and its mRNA transcription; 2) engagement of CD44 up-regulated Fas on the cells within 3 h, much more than IL-1beta and TNF-alpha did; 3) the Fas-mediated early apoptotic change of the cells was amplified by CD44 cross-linking; and 4) hyaluronan, especially when fragmented, also augmented Fas-mediated early apoptosis of the cells. Based on these findings, we postulate a new concept: that interaction of CD44 on RA synovial cells with hyaluronan fragments present in the surrounding extracellular matrix augments Fas expression as well as Fas-mediated apoptosis of synovial cells. This may lead to spontaneous growth arrest through Fas-Fas ligand pathway observed in synovial cells of RA synovitis in vivo. | lld:pubmed |
pubmed-article:11466334 | pubmed:language | eng | lld:pubmed |
pubmed-article:11466334 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11466334 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:11466334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11466334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11466334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11466334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11466334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:11466334 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11466334 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11466334 | pubmed:month | Aug | lld:pubmed |
pubmed-article:11466334 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:11466334 | pubmed:author | pubmed-author:TanakaYY | lld:pubmed |
pubmed-article:11466334 | pubmed:author | pubmed-author:FujiiKK | lld:pubmed |
pubmed-article:11466334 | pubmed:author | pubmed-author:FujiiYY | lld:pubmed |
pubmed-article:11466334 | pubmed:author | pubmed-author:HubscherSS | lld:pubmed |
pubmed-article:11466334 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11466334 | pubmed:day | 1 | lld:pubmed |
pubmed-article:11466334 | pubmed:volume | 167 | lld:pubmed |
pubmed-article:11466334 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11466334 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11466334 | pubmed:pagination | 1198-203 | lld:pubmed |
pubmed-article:11466334 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:11466334 | pubmed:meshHeading | pubmed-meshheading:11466334... | lld:pubmed |
pubmed-article:11466334 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11466334 | pubmed:articleTitle | CD44 is the physiological trigger of Fas up-regulation on rheumatoid synovial cells. | lld:pubmed |
pubmed-article:11466334 | pubmed:affiliation | First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan. | lld:pubmed |
pubmed-article:11466334 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11466334 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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