Source:http://linkedlifedata.com/resource/pubmed/id/19700629
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2009-10-22
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| pubmed:abstractText |
Advanced glycation end product (AGE) subtypes, proteins or lipids that become glycated after exposure to sugars, induce complications in diabetes. Among the various AGE subtypes, glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) have been indicated to play roles in inflammation in diabetic patients. The engagement of AGEs and receptor for AGEs activates monocytes. Because the engagement of intercellular adhesion molecule-1 (ICAM-1), B7.1, B7.2, and CD40 on monocytes with their ligands on T cells plays roles in cytokine production, we investigated the effects of AGE-2 and AGE-3 on the expressions of ICAM-1, B7.1, B7.2, and CD40 on monocytes, the production of interferon gamma and tumor necrosis factor alpha, and the lymphocyte proliferation in human peripheral blood mononuclear cells and their modulation by prostaglandin E(2) (PGE(2)). AGE-2 and AGE-3 induced the expressions of adhesion molecule, the cytokine production, and the lymphocyte proliferation. PGE(2) concentration-dependently inhibited the actions of AGE-2 and AGE-3. The effects of PGE(2) were mimicked by an E-prostanoid (EP)(2)-receptor agonist, 11,15-O-dimethyl prostaglandin E(2) (ONO-AE1-259-01), and an EP(4) receptor agonist, 16-(3-methoxymethyl)phenyl-omega-tetranor-3,7-dithia prostaglandin E(1) (ONO-AE1-329). An EP(2)-receptor antagonist, 6-isopropoxy-9-oxaxanthene-2-carboxylic acid (AH6809), and an EP(4)-receptor antagonist, (4Z)-7-[(rel-1S,2S,5R)-5-(1,1'-biphenyl-4-yl)methoxy)-2-(4-morpholinyl)-3-oxocyclopentyl]-4-heptenoic acid (AH23848), inhibited the actions of PGE(2). The stimulation of EP(2) and EP(4) receptors is reported to increase cAMP levels. The effects of PGE(2) were reversed by a protein kinase A (PKA) inhibitor, H89, and mimicked by a dibutyryl cAMP and an adenylate cyclase activator, forskolin. These results as a whole indicated that PGE(2) inhibited the actions of AGE-2 and AGE-3 via EP(2)/EP(4) receptors and the cAMP/PKA pathway.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/Bucladesine,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP-Dependent Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone,
http://linkedlifedata.com/resource/pubmed/chemical/Forskolin,
http://linkedlifedata.com/resource/pubmed/chemical/Glycosylation End Products, Advanced,
http://linkedlifedata.com/resource/pubmed/chemical/Isoquinolines,
http://linkedlifedata.com/resource/pubmed/chemical/N-(2-(4-bromocinnamylamino)ethyl)-5-...,
http://linkedlifedata.com/resource/pubmed/chemical/PTGER2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/PTGER4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Prostaglandin E,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Prostaglandin E, EP2...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Prostaglandin E, EP4...,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfonamides
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| pubmed:status |
MEDLINE
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| pubmed:month |
Nov
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| pubmed:issn |
1521-0103
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
331
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
656-70
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| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:19700629-Adenylate Cyclase,
pubmed-meshheading:19700629-Bucladesine,
pubmed-meshheading:19700629-Cell Adhesion Molecules,
pubmed-meshheading:19700629-Cell Proliferation,
pubmed-meshheading:19700629-Cell Separation,
pubmed-meshheading:19700629-Cyclic AMP,
pubmed-meshheading:19700629-Cyclic AMP-Dependent Protein Kinases,
pubmed-meshheading:19700629-Cytokines,
pubmed-meshheading:19700629-Dinoprostone,
pubmed-meshheading:19700629-Enzyme Activation,
pubmed-meshheading:19700629-Flow Cytometry,
pubmed-meshheading:19700629-Forskolin,
pubmed-meshheading:19700629-Glycosylation End Products, Advanced,
pubmed-meshheading:19700629-Humans,
pubmed-meshheading:19700629-Isoquinolines,
pubmed-meshheading:19700629-Lymphocytes,
pubmed-meshheading:19700629-Monocytes,
pubmed-meshheading:19700629-Receptors, Prostaglandin E,
pubmed-meshheading:19700629-Receptors, Prostaglandin E, EP2 Subtype,
pubmed-meshheading:19700629-Receptors, Prostaglandin E, EP4 Subtype,
pubmed-meshheading:19700629-Sulfonamides
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| pubmed:year |
2009
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| pubmed:articleTitle |
Prostaglandin E2 inhibits advanced glycation end product-induced adhesion molecule expression, cytokine production, and lymphocyte proliferation in human peripheral blood mononuclear cells.
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| pubmed:affiliation |
Department of Pharmacology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
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| pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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