University of Hertfordshire

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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. / 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.

In: FASEB Journal, Vol. 27, 10.2013, p. 3938-46.

Research output: Contribution to journalArticle

Harvard

Kirkby, N, Chan, MV, Lundberg, MH, MacKenzie, L, Leadbeater, PDM, Milne, GL, Potter, CM, Al-Yamani, M, Adeyemi, O, Warner, TD & Mitchell, JA 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

APA

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, 27, 3938-46. https://doi.org/10.1096/fj.12-215533

Vancouver

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. / 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. In: FASEB Journal. 2013 ; Vol. 27. pp. 3938-46.

Bibtex

@article{5306d14e245e4b2abc2b0b8cd429c865,
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",
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",
author = "Nick Kirkby and M.V. Chan and M.H. Lundberg and Louise MacKenzie and Leadbeater, {Phillip D.M.} and Milne, {Ginger L.} and Potter, {Claire M.} and Malak Al-Yamani and Oladipupo Adeyemi and Warner, {Tim D.} and Mitchell, {Jane A.}",
year = "2013",
month = oct,
doi = "10.1096/fj.12-215533",
language = "English",
volume = "27",
pages = "3938--46",
journal = "FASEB Journal",
issn = "0892-6638",
publisher = "FASEB",

}

RIS

TY - JOUR

T1 - Aspirin triggered 15-epi-lipoxin A4 predicts cyclo-oxygenase-2 in the lungs of LPS treated mice but not in the circulation

T2 - implications for a clinical test

AU - Kirkby, Nick

AU - Chan, M.V.

AU - Lundberg, M.H.

AU - MacKenzie, Louise

AU - Leadbeater, Phillip D.M.

AU - Milne, Ginger L.

AU - Potter, Claire M.

AU - Al-Yamani, Malak

AU - Adeyemi, Oladipupo

AU - Warner, Tim D.

AU - Mitchell, Jane A.

PY - 2013/10

Y1 - 2013/10

N2 - 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

AB - 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

U2 - 10.1096/fj.12-215533

DO - 10.1096/fj.12-215533

M3 - Article

VL - 27

SP - 3938

EP - 3946

JO - FASEB Journal

JF - FASEB Journal

SN - 0892-6638

ER -