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

Asai, Akira; Okajima, Fumitaka; Nakagawa, Kiyotaka; Ibusuki, Daigo; Tanimura-Inagaki, Kyoko; Nakajima, Yasushi; Nagao, Mototsugu LU ; Sudo, Mariko; Harada, Taro and Miyazawa, Teruo, et al. (2009) In Journal of Lipid Research 50(5). p.65-957
Abstract

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... (More)

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.

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keywords
Actins, Antigens, CD, Cell Adhesion, Cell Line, Cell Surface Extensions, Cytochalasin D, Cytoskeleton, Endothelial Cells, Humans, Intercellular Adhesion Molecule-1, Lymphocyte Function-Associated Antigen-1, Monocytes, Nucleic Acid Synthesis Inhibitors, Oxidation-Reduction, Phosphatidylcholines, Reactive Oxygen Species, Journal Article, Research Support, Non-U.S. Gov't
in
Journal of Lipid Research
volume
50
issue
5
pages
9 pages
publisher
American Society for Biochemistry and Molecular Biology
external identifiers
  • scopus:67649716591
ISSN
0022-2275
DOI
10.1194/jlr.M800582-JLR200
language
English
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no
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73c987d8-896a-41c1-8768-7303619959a8
date added to LUP
2017-08-24 20:58:40
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2017-08-28 15:17:19
@article{73c987d8-896a-41c1-8768-7303619959a8,
  abstract     = {<p>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.</p>},
  author       = {Asai, Akira and Okajima, Fumitaka and Nakagawa, Kiyotaka and Ibusuki, Daigo and Tanimura-Inagaki, Kyoko and Nakajima, Yasushi and Nagao, Mototsugu and Sudo, Mariko and Harada, Taro and Miyazawa, Teruo and Oikawa, Shinichi},
  issn         = {0022-2275},
  keyword      = {Actins,Antigens, CD,Cell Adhesion,Cell Line,Cell Surface Extensions,Cytochalasin D,Cytoskeleton,Endothelial Cells,Humans,Intercellular Adhesion Molecule-1,Lymphocyte Function-Associated Antigen-1,Monocytes,Nucleic Acid Synthesis Inhibitors,Oxidation-Reduction,Phosphatidylcholines,Reactive Oxygen Species,Journal Article,Research Support, Non-U.S. Gov't},
  language     = {eng},
  number       = {5},
  pages        = {65--957},
  publisher    = {American Society for Biochemistry and Molecular Biology},
  series       = {Journal of Lipid Research},
  title        = {Phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to intracellular adhesion molecule-1},
  url          = {http://dx.doi.org/10.1194/jlr.M800582-JLR200},
  volume       = {50},
  year         = {2009},
}