Source:http://linkedlifedata.com/resource/pubmed/id/11342653
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
2001-5-8
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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.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Annexins,
http://linkedlifedata.com/resource/pubmed/chemical/Dexamethasone,
http://linkedlifedata.com/resource/pubmed/chemical/L-Selectin,
http://linkedlifedata.com/resource/pubmed/chemical/Metalloendopeptidases,
http://linkedlifedata.com/resource/pubmed/chemical/N-Formylmethionine...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Formyl Peptide,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Peptide,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
166
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6294-300
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11342653-Animals,
pubmed-meshheading:11342653-Annexins,
pubmed-meshheading:11342653-Cattle,
pubmed-meshheading:11342653-Cell Size,
pubmed-meshheading:11342653-Dexamethasone,
pubmed-meshheading:11342653-Dose-Response Relationship, Immunologic,
pubmed-meshheading:11342653-Down-Regulation,
pubmed-meshheading:11342653-Flow Cytometry,
pubmed-meshheading:11342653-Humans,
pubmed-meshheading:11342653-L-Selectin,
pubmed-meshheading:11342653-Leukocytes,
pubmed-meshheading:11342653-Metalloendopeptidases,
pubmed-meshheading:11342653-Myeloid Cells,
pubmed-meshheading:11342653-N-Formylmethionine Leucyl-Phenylalanine,
pubmed-meshheading:11342653-Neutrophil Activation,
pubmed-meshheading:11342653-Receptors, Formyl Peptide,
pubmed-meshheading:11342653-Receptors, Immunologic,
pubmed-meshheading:11342653-Receptors, Peptide,
pubmed-meshheading:11342653-Tetradecanoylphorbol Acetate
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pubmed:year |
2001
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pubmed:articleTitle |
A potential role for annexin 1 as a physiologic mediator of glucocorticoid-induced L-selectin shedding from myeloid cells.
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pubmed:affiliation |
Department of Anatomy, Program in Immunology and Cardiovascular Research Institute, University of California, San Francisco, CA 94143, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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