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J. Lipid Res.
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A more recent version of this article appeared on October 1, 2008

Papers In Press, published online ahead of print June 27, 2008
J. Lipid Res., doi:10.1194/jlr.M800188-JLR200
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Submitted on April 17, 2008
Revised on June 27, 2008
Accepted on June 27, 2008

Platelet-activating factor acetylhydrolase and transacetylase activities in human aorta and mammary artery

Demokritos C. Tsoukatos, Isabelle Brochériou, Vassilios Moussis, Christina P. Panopoulou, Elena D. Christofidou, Stamatis Koussissis, Socratis Sismanidis, Ewa Ninio, and Stavros Siminelakis

Chemistry, University of Ioannina, Ioannina, Ioannina 45110

Corresponding Author: dtsoykat{at}cc.uoi.gr

Platelet-activating factor (PAF), the potent phospholipid mediator of inflammation is involved in atherosclerosis. Platelet-activating factor-acetylhydrolase (PAF-AH), the enzyme that inactivates PAF-bioactivity, possesses both acetylhydrolase and transacetylase activities. In the present study we measured acetylhydrolase and transacetylase activities in human atherogenic aorta and non-atherogenic mammary arteries. Immunohistochemistry analysis showed PAF-AH expression in the intima and the media of the aorta and in the media of mammary arteries. Acetylhydrolase and transacetylase activities were (mean ± SE n=38): acetylhydrolase of aorta: 2.8 ± 0.5 pmol/min/mg of tissue; transacetylase of aorta: 3.3 ± 0.7 pmol/min/mg of tissue; acetylhydrolase of mammary artery: 1.4 ± 0.3* pmol/min/mg of tissue; transacetylase of mammary artery: 0.8 ± 0.2** pmol/min/mg of tissue. (* P<0.004 as compared with acetylhydrolase of aorta; ** P<0.03 as compared with acetylhydrolase of mammary artery). Lyso PAF accumulation and an increase in PAF-bioactivity were observed in the aorta of some patients. RP-HPLC and ESI-MS analysis revealed that 1-O-hexadecyl-2 acetyl-sn glycero-3-phosphocholine accounted for 60% of the PAF-bioactivity and 1-O-hexadecyl-2-butanoyl-sn-glycerol-3-phosphocholine for 40% of the PAF-bioactivity. Conclusion: The non-atherogenic properties of mammary arteries may in part be due to low PAF formation regulated by PAF-acetylhydrolase activity. In atherogenic aortas, an imbalance between PAF-acetylhydrolase and transacetylase activity, as well as lyso PAF accumulation, may lead to unregulated PAF formation and to progression of atherosclerosis.


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