| pubmed-article:11342653 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11342653 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:11342653 | lifeskim:mentions | umls-concept:C0035647 | lld:lifeskim |
| pubmed-article:11342653 | lifeskim:mentions | umls-concept:C0887899 | lld:lifeskim |
| pubmed-article:11342653 | lifeskim:mentions | umls-concept:C0125090 | lld:lifeskim |
| pubmed-article:11342653 | lifeskim:mentions | umls-concept:C2361980 | lld:lifeskim |
| pubmed-article:11342653 | lifeskim:mentions | umls-concept:C0205463 | lld:lifeskim |
| pubmed-article:11342653 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
| pubmed-article:11342653 | lifeskim:mentions | umls-concept:C1363844 | lld:lifeskim |
| pubmed-article:11342653 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:11342653 | pubmed:dateCreated | 2001-5-8 | lld:pubmed |
| pubmed-article:11342653 | pubmed:abstractText | Glucocorticoids can dampen inflammatory responses by inhibiting neutrophil recruitment to tissue sites. The detailed mechanism by which glucocorticoids exert this affect on neutrophils is unknown. L-selectin is a leukocyte cell surface receptor that is implicated in several steps of neutrophil recruitment. Recently, several studies have shown that systemic treatment of animals and humans with glucocorticoids induces decreased L-selectin expression on neutrophils, suggesting one mechanism by which inflammation may be negatively regulated. However, when neutrophils are treated in vitro with glucocorticoids, no effect on L-selectin expression is observed. Thus, the existence of an additional mediator is plausible. In this study, we investigate whether annexin 1 (ANX1), a recognized second messenger of glucocorticoids, could be such a mediator. We show that ANX1 induces a dose- and time-dependent decrease in L-selectin expression on both peripheral blood neutrophils and monocytes but has no effect on lymphocytes. The loss of L-selectin from neutrophils is due to shedding that is mediated by a cell surface metalloprotease ("sheddase"). Using cell shape and a beta(2) integrin activation epitope, we show that the ANX1-induced shedding of L-selectin appears to occur without overt cell activation. These data may provide the basis for further understanding of mechanisms involved in the down-regulation of inflammatory responses. | lld:pubmed |
| pubmed-article:11342653 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342653 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11342653 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342653 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:11342653 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342653 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342653 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342653 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342653 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342653 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342653 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11342653 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11342653 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11342653 | pubmed:month | May | lld:pubmed |
| pubmed-article:11342653 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:11342653 | pubmed:author | pubmed-author:RosenS DSD | lld:pubmed |
| pubmed-article:11342653 | pubmed:author | pubmed-author:StrausbaughH... | lld:pubmed |
| pubmed-article:11342653 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11342653 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:11342653 | pubmed:volume | 166 | lld:pubmed |
| pubmed-article:11342653 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11342653 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11342653 | pubmed:pagination | 6294-300 | lld:pubmed |
| pubmed-article:11342653 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:11342653 | pubmed:meshHeading | pubmed-meshheading:11342653... | lld:pubmed |
| pubmed-article:11342653 | pubmed:meshHeading | pubmed-meshheading:11342653... | lld:pubmed |
| pubmed-article:11342653 | pubmed:meshHeading | pubmed-meshheading:11342653... | lld:pubmed |
| pubmed-article:11342653 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11342653 | pubmed:articleTitle | A potential role for annexin 1 as a physiologic mediator of glucocorticoid-induced L-selectin shedding from myeloid cells. | lld:pubmed |
| pubmed-article:11342653 | pubmed:affiliation | Department of Anatomy, Program in Immunology and Cardiovascular Research Institute, University of California, San Francisco, CA 94143, USA. | lld:pubmed |
| pubmed-article:11342653 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11342653 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11342653 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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