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.