pubmed-article:20972877 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20972877 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
pubmed-article:20972877 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:20972877 | lifeskim:mentions | umls-concept:C0003847 | lld:lifeskim |
pubmed-article:20972877 | lifeskim:mentions | umls-concept:C1522318 | lld:lifeskim |
pubmed-article:20972877 | lifeskim:mentions | umls-concept:C0068355 | lld:lifeskim |
pubmed-article:20972877 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:20972877 | lifeskim:mentions | umls-concept:C1539608 | lld:lifeskim |
pubmed-article:20972877 | lifeskim:mentions | umls-concept:C1414506 | lld:lifeskim |
pubmed-article:20972877 | lifeskim:mentions | umls-concept:C1417826 | lld:lifeskim |
pubmed-article:20972877 | lifeskim:mentions | umls-concept:C1998811 | lld:lifeskim |
pubmed-article:20972877 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:20972877 | pubmed:dateCreated | 2010-12-30 | lld:pubmed |
pubmed-article:20972877 | pubmed:abstractText | Protease-activated receptor-2 (PAR2) is expressed in endothelial cells and mediates endothelium-dependent vasodilation. We hypothesized that PAR2 regulates tumor necrosis factor-alpha (TNF-?)-induced coronary arteriolar dysfunction in type 2 diabetic (db/db) mice. To test this, coronary arterioles from WT control, db/db, db/db mice treated with PAR2 antagonist FSLLRY-NH? (db/db+FSLLRY-NH?) and db/db mice null for TNF (db(TNF-)/db(TNF-)) were isolated and pressurized (60 cmH?O) without flow. Although vasodilation to the endothelium-independent vasodilator sodium nitroprusside (SNP) was not different among WT, db/db, db/db+FSLLRY-NH? and db(TNF-)/db(TNF-), endothelium-dependent acetylcholine (ACh)- and flow-mediated vasodilation were impaired in db/db mice but were enhanced in db(TNF-)/db(TNF-) mice and db/db mice treated with PAR2 antagonist. NOS inhibitor N (G)-nitro-L-arginine-methyl ester (L-NAME) significantly reduced ACh-induced dilation in WT, db(TNF-)/db(TNF-) and db/db+FSLLRY-NH?, but did not alter the vasodilation in db/db mice. In contrast, cyclooxygenase (COX) inhibitor indomethacin (Indo) did not alter ACh-induced vasodilation in these four groups of mice. PAR2-activating peptide (PAR2-AP, 2-Furoyl-LIGRLO-am)-induced dilation was higher in db/db mice than that in WT, db(TNF-)/db(TNF-) and db/db mice treated with PAR2 antagonist. These effects were abolished by denudation, or in the presence of L-NAME or Indo. Protein expressions of TNF-?, PAR2, gp91(phox) and p47(phox) in the heart and isolated coronary arterioles were higher in db/db mice compared to WT mice. Administration of PAR2 antagonist to db/db mice reduced protein expression of TNF-?, gp91(phox) and PAR2. Protein expression of gp91(phox) and p47(phox) was lower in db(TNF-)/db(TNF-) compared to db/db mice. These results indicate that PAR2 plays a pivotal role in endothelial dysfunction in type 2 diabetes by up-regulating the expression/production of TNF-? and activating NAD(P)H oxidase subunit p47(phox). | lld:pubmed |
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pubmed-article:20972877 | pubmed:language | eng | lld:pubmed |
pubmed-article:20972877 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20972877 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:20972877 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:20972877 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20972877 | pubmed:month | Jan | lld:pubmed |
pubmed-article:20972877 | pubmed:issn | 1435-1803 | lld:pubmed |
pubmed-article:20972877 | pubmed:author | pubmed-author:YangJiyeonJ | lld:pubmed |
pubmed-article:20972877 | pubmed:author | pubmed-author:ZhangCuihuaC | lld:pubmed |
pubmed-article:20972877 | pubmed:author | pubmed-author:ParkYoonjungY | lld:pubmed |
pubmed-article:20972877 | pubmed:author | pubmed-author:ZhangHanruiH | lld:pubmed |
pubmed-article:20972877 | pubmed:author | pubmed-author:ChenXiaonaiX | lld:pubmed |
pubmed-article:20972877 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20972877 | pubmed:volume | 106 | lld:pubmed |
pubmed-article:20972877 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20972877 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20972877 | pubmed:pagination | 111-23 | lld:pubmed |
pubmed-article:20972877 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
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