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J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.M800582-JLR200 on December 29, 2008

Papers In Press, published online ahead of print May 1, 2009
J. Lipid Res., doi:10.1194/jlr.M800582-JLR200
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Journal of Lipid Research, Vol. 50, 957-965, May 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to intracellular adhesion molecule-1boxs

Akira Asai*, Fumitaka Okajima*, Kiyotaka Nakagawa{dagger}, Daigo Ibusuki{dagger}, Kyoko Tanimura*, Yasushi Nakajima*, Mototsugu Nagao*, Mariko Sudo*, Taro Harada*, Teruo Miyazawa{dagger} and Shinichi Oikawa1,*

* Division of Endocrinology and Metabolism, Department of Medicine, Nippon Medical School, Tokyo 113-8603, Japan
{dagger} Food and Biodynamic Chemistry Laboratory, Graduate School of Agricultural Science, Tohoku University, Sendai 981-8555, Japan

boxs The online version of this article (available at http://www.jlr.org) contains supplementary data in the form of four figures.

This research was supported in part by Grants-in-Aid from the Bio-oriented Technology Research Advancement Center of the National Agricultural and Biological Research Organization and from the Japanese Ministry of Education, Science, Sport, and Culture (18591005 to S.O.).

Published, JLR Papers in Press, December 29, 2009.

1 To whom correspondence should be addressed. e-mail: shinichi{at}nms.ac.jp

The accumulation of phosphatidylcholine hydroperoxide (PCOOH), a primary oxidation product of phosphatidylcholine (PC), in blood plasma and tissues has been observed in various pathological conditions, including atherosclerosis. However, the biological roles of PCOOH in these conditions remain unknown. To estimate the atherogenicity of PCOOH, we evaluated the effect of PCOOH on THP-1 monocytic cell adherence to immobilized vascular endothelial cell adhesion molecules. THP-1 cell adhesion to intracellular adhesion molecule-1 (ICAM-1) was dose-dependently increased by addition of PCOOH. Phosphatidylcholine hydroxide (a hydroxyl analog of PCOOH) also induced THP-1 cell adhesion to ICAM-1, whereas nonoxidized PC, sn-2 truncated PCs, and other hydroperoxide compounds did not affect the adhesion. In the PCOOH-treated cells, obvious protruding F-actin-rich membrane structures were formed, and lymphocyte function-associated antigen-1 (LFA-1) was localized to the protruding structures. Cytochalasin D, an actin polymerization inhibitor, suppressed the PCOOH-induced cell adhesion to ICAM-1 and the membrane protrusions. These results indicate that PCOOH evokes LFA-1-mediated cell adhesion to ICAM-1 via actin cytoskeletal organization, and the mechanism may participate in monocyte adherence to the arterial wall in the initiation of atherosclerosis.

Supplementary key words lipid oxidation • phospholipid • atherosclerosis • monocyte • integrin • cell adhesion molecule • actin cytoskeleton

Abbreviations: HNE, 4-hydroxy-2-nonenal; H(p)ETE, hydro(pero)xyeicosatetraenoic acid; H(p)ODE, hydro(pero)xyoctadecadienoic acid; ICAM-1, intracellular adhesion molecule-1; LFA-1, lymphocyte function-associated antigen-1; LysoPC, lysophosphatidylcholine; mAb24, monoclonal antibody 24; PAPC, 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine; PAPCO(O)H, PAPC hydro(pero)xide; PC, phosphatidylcholine; PCOH, phosphatidylcholine hydroxide; PCOOH, phosphatidylcholine hydroperoxide; PKC, protein kinase C; PLA2, phospholipase A2; PLPC, 1-palmitoyl-2-linoleoyl-sn-glycero-3-phosphocholine; PLPCO(O)H, PLPC hydro(pero)xide; POVPC, 1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine; ROS, reactive oxygen species; VCAM-1, vascular cell adhesion molecule-1


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