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        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

        Author
        Kirkby, Nick
        Chan, M.V.
        Lundberg, M.H.
        MacKenzie, Louise
        Leadbeater, Phillip D.M.
        Milne, Ginger L.
        Potter, Claire M.
        Al-Yamani, Malak
        Adeyemi, Oladipupo
        Warner, Tim D.
        Mitchell, Jane A.
        Attention
        2299/12092
        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
        Publication date
        2013-10
        Published in
        FASEB Journal
        Published version
        https://doi.org/10.1096/fj.12-215533
        Other links
        http://hdl.handle.net/2299/12092
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