| pubmed-article:10202042 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10202042 | lifeskim:mentions | umls-concept:C0014257 | lld:lifeskim |
| pubmed-article:10202042 | lifeskim:mentions | umls-concept:C2917210 | lld:lifeskim |
| pubmed-article:10202042 | lifeskim:mentions | umls-concept:C1516019 | lld:lifeskim |
| pubmed-article:10202042 | lifeskim:mentions | umls-concept:C0599894 | lld:lifeskim |
| pubmed-article:10202042 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
| pubmed-article:10202042 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:10202042 | pubmed:dateCreated | 1999-5-6 | lld:pubmed |
| pubmed-article:10202042 | pubmed:abstractText | The complement inhibitor soluble complement receptor type 1 (sCR1) and a truncated form of sCR1, sCR1[desLHR-A], have been generated with expression of the selectin-reactive oligosaccharide moiety, sialyl Lewisx (sLex), as N-linked oligosaccharide adducts. These modified proteins, sCR1sLex and sCR1[desLHR-A]sLex, were assessed in the L-selectin- and P-selectin-dependent rat model of lung injury following systemic activation of complement by cobra venom factor and in the L-selectin-, P-selectin-, and E-selectin-dependent model of lung injury following intrapulmonary deposition of IgG immune complexes. In the cobra venom factor model, sCR1sLex and sCR1[desLHR-A]sLex caused substantially greater reductions in neutrophil accumulation and in albumin extravasation in lung when compared with the non-sLex-decorated forms. In this model, increased lung vascular binding of sCR1sLex and sCR1[desLHR-A]sLex occurred in a P-selectin-dependent manner, in contrast to the absence of any increased binding of sCR1 or sCR1[desLHR-A]. In the IgG immune complex model, sCR1[desLHR-A]sLex possessed greater protective effects relative to sCR1[desLHR-A], based on albumin extravasation and neutrophil accumulation. Enhanced protective effects correlated with greater lung vascular binding of sCR1[desLHR-A]sLex as compared with the non-sLex-decorated form. In TNF-alpha-activated HUVEC, substantial in vitro binding occurred with sCR1[desLHR-A]sLex (but not with sCR1[desLHR-A]). This endothelial cell binding was blocked by anti-E-selectin but not by anti-P-selectin. These data suggest that sLex-decorated complement inhibitors have enhanced antiinflammatory effects and appear to have enhanced ability to localize to the activated vascular endothelium. | lld:pubmed |
| pubmed-article:10202042 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10202042 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10202042 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10202042 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10202042 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:10202042 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:10202042 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10202042 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:10202042 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:10202042 | pubmed:author | pubmed-author:WardP APA | lld:pubmed |
| pubmed-article:10202042 | pubmed:author | pubmed-author:RyanU SUS | lld:pubmed |
| pubmed-article:10202042 | pubmed:author | pubmed-author:WarnerR LRL | lld:pubmed |
| pubmed-article:10202042 | pubmed:author | pubmed-author:ThomasL JLJ | lld:pubmed |
| pubmed-article:10202042 | pubmed:author | pubmed-author:RittershausC... | lld:pubmed |
| pubmed-article:10202042 | pubmed:author | pubmed-author:MulliganM SMS | lld:pubmed |
| pubmed-article:10202042 | pubmed:author | pubmed-author:TillG OGO | lld:pubmed |
| pubmed-article:10202042 | pubmed:author | pubmed-author:ForemanK EKE | lld:pubmed |
| pubmed-article:10202042 | pubmed:author | pubmed-author:CrouchL DLD | lld:pubmed |
| pubmed-article:10202042 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10202042 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:10202042 | pubmed:volume | 162 | lld:pubmed |
| pubmed-article:10202042 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10202042 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10202042 | pubmed:pagination | 4952-9 | lld:pubmed |
| pubmed-article:10202042 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:10202042 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10202042 | pubmed:articleTitle | Endothelial targeting and enhanced antiinflammatory effects of complement inhibitors possessing sialyl Lewisx moieties. | lld:pubmed |
| pubmed-article:10202042 | pubmed:affiliation | Department of Surgery and Pathology, University of Michigan Medical School, Ann Arbor 48109, USA. | lld:pubmed |
| pubmed-article:10202042 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10202042 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:10202042 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10202042 | lld:pubmed |
