dc.contributor.author | Kirkby, Nick | |
dc.contributor.author | Chan, M.V. | |
dc.contributor.author | Lundberg, M.H. | |
dc.contributor.author | MacKenzie, Louise | |
dc.contributor.author | Leadbeater, Phillip D.M. | |
dc.contributor.author | Milne, Ginger L. | |
dc.contributor.author | Potter, Claire M. | |
dc.contributor.author | Al-Yamani, Malak | |
dc.contributor.author | Adeyemi, Oladipupo | |
dc.contributor.author | Warner, Tim D. | |
dc.contributor.author | Mitchell, Jane A. | |
dc.date.accessioned | 2013-11-07T10:30:58Z | |
dc.date.available | 2013-11-07T10:30:58Z | |
dc.date.issued | 2013-10 | |
dc.identifier.citation | Kirkby , N , Chan , M V , Lundberg , M H , MacKenzie , L , Leadbeater , P D M , Milne , G L , Potter , C M , Al-Yamani , M , Adeyemi , O , Warner , T D & Mitchell , J A 2013 , ' Aspirin triggered 15-epi-lipoxin A4 predicts cyclo-oxygenase-2 in the lungs of LPS treated mice but not in the circulation : implications for a clinical test ' , FASEB Journal , vol. 27 , pp. 3938-46 . https://doi.org/10.1096/fj.12-215533 | |
dc.identifier.issn | 0892-6638 | |
dc.identifier.other | PURE: 1972009 | |
dc.identifier.other | PURE UUID: 5306d14e-245e-4b2a-bc2b-0b8cd429c865 | |
dc.identifier.other | Scopus: 84885130079 | |
dc.identifier.uri | http://hdl.handle.net/2299/12092 | |
dc.description.abstract | Inhibition of cyclooxygenase (COX)-2 increases cardiovascular deaths. Identifying a biomarker of COX-2 is desirable but difficult, since COX-1 and COX-2 ordinarily catalyze formation of an identical product, prostaglandin H2. When acetylated by aspirin, however, COX-2 (but not COX-1) can form 15(R)-HETE, which is metabolized to aspirin-triggered lipoxin (ATL), 15-epi-lipoxin A4. Here we have used COX-1- and COX-2-knockout mice to establish whether plasma ATL could be used as a biomarker of vascular COX-2 in vivo. Vascular COX-2 was low but increased by LPS (10 mg/kg; i.p). Aspirin (10 mg/kg; i.v.) inhibited COX-1, measured as blood thromboxane and COX-2, measured as lung PGE2. Aspirin also increased the levels of ATL in the lungs of LPS-treated wild-type C57Bl6 mice (vehicle: 25.5±9.3 ng/ml; 100 mg/kg: 112.0±7.4 ng/ml; P<0.05). Despite this, ATL was unchanged in plasma after LPS and aspirin. This was true in wild-type as well as COX-1-/- and COX-2-/- mice. Thus, in mice in which COX-2 has been induced by LPS treatment, aspirin triggers detectable 15-epi-lipoxin A4 in lung tissue, but not in plasma. This important study is the first to demonstrate that while ATL can be measured in tissue, plasma ATL is not a biomarker of vascular COX-2 expression | en |
dc.language.iso | eng | |
dc.relation.ispartof | FASEB Journal | |
dc.title | Aspirin triggered 15-epi-lipoxin A4 predicts cyclo-oxygenase-2 in the lungs of LPS treated mice but not in the circulation : implications for a clinical test | en |
dc.contributor.institution | School of Life and Medical Sciences | |
dc.contributor.institution | Health & Human Sciences Research Institute | |
dc.contributor.institution | Department of Human and Environmental Sciences | |
dc.contributor.institution | Pharmacology and Clinical Science Research | |
dc.contributor.institution | Agriculture, Food and Veterinary Sciences | |
dc.contributor.institution | Cardiovascular Pathologies | |
dc.contributor.institution | Diabetic neuropathies | |
dc.description.status | Peer reviewed | |
rioxxterms.versionofrecord | https://doi.org/10.1096/fj.12-215533 | |
rioxxterms.type | Journal Article/Review | |
herts.preservation.rarelyaccessed | true | |