| pubmed-article:12225971 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12225971 | lifeskim:mentions | umls-concept:C0014124 | lld:lifeskim |
| pubmed-article:12225971 | lifeskim:mentions | umls-concept:C0600434 | lld:lifeskim |
| pubmed-article:12225971 | lifeskim:mentions | umls-concept:C1155002 | lld:lifeskim |
| pubmed-article:12225971 | lifeskim:mentions | umls-concept:C0719453 | lld:lifeskim |
| pubmed-article:12225971 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:12225971 | pubmed:dateCreated | 2002-9-12 | lld:pubmed |
| pubmed-article:12225971 | pubmed:abstractText | To determine whether homocysteine (Hcy)-mediated activation of endocardial endothelial (EE) cells is ameliorated by peroxisome proliferator-activated receptor (PPAR), we isolated EE cells from mouse endocardium. Matrix metalloproteinase (MMP) activity and intercellular adhesion molecule (ICAM)-1 in EE cells were measured in the presence and absence of Hcy, and ciprofibrate (CF; PPAR-alpha agonist) or 15-deoxy-Delta(12,14)-prostaglandin J(2) (PGJ(2); PPAR-gamma agonist) by zymography and Western blot analyses, respectively. Results suggest that Hcy-mediated MMP activation and ICAM-1 expression are ameliorated by CF and PGJ(2). To test the hypothesis that Hcy competes with other ligands for binding to PPARalpha and -gamma, we prepared cardiac nuclear extracts. Extracts were loaded onto an Hcy-cellulose affinity column. Bound proteins were eluted with CF and PGJ(2). To determine conformational changes in PPAR upon binding to Hcy, we measured PPAR fluorescence at 334 nm. Dose-dependent increase in PPAR fluorescence demonstrated a primary binding affinity of 0.32 +/- 0.06 microM. There was dose-dependent quenching of PPAR fluorescence by fluorescamine-homocysteine (F-Hcy). PPAR-alpha fluorescence quenching was abrogated by the addition of CF but not by PGJ(2). PPAR-gamma fluorescence quenching was abrogated by the addition of PGJ(2) but not by CF. These results suggest that Hcy competes with CF and PGJ(2) for binding to PPAR-alpha and -gamma, respectively, indicating a role of PPAR in amelioration of Hcy-mediated EE dysfunction. | lld:pubmed |
| pubmed-article:12225971 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:12225971 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12225971 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12225971 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12225971 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12225971 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:12225971 | pubmed:issn | 0363-6143 | lld:pubmed |
| pubmed-article:12225971 | pubmed:author | pubmed-author:TyagiSuresh... | lld:pubmed |
| pubmed-article:12225971 | pubmed:author | pubmed-author:HuntMatthew... | lld:pubmed |
| pubmed-article:12225971 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12225971 | pubmed:volume | 283 | lld:pubmed |
| pubmed-article:12225971 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12225971 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12225971 | pubmed:pagination | C1073-9 | lld:pubmed |
| pubmed-article:12225971 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:12225971 | pubmed:meshHeading | pubmed-meshheading:12225971... | lld:pubmed |
| pubmed-article:12225971 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12225971 | pubmed:articleTitle | Peroxisome proliferators compete and ameliorate Hcy-mediated endocardial endothelial cell activation. | lld:pubmed |
| pubmed-article:12225971 | pubmed:affiliation | Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, USA. | lld:pubmed |
| pubmed-article:12225971 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12225971 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12225971 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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