Journal of Biochemistry Advance Access originally published online on October 30, 2008
Journal of Biochemistry 2009 145(1):43-50; doi:10.1093/jb/mvn139
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Inhibitory effect of N-palmitoylphosphatidylethanolamine on macrophage phagocytosis through inhibition of Rac1 and Cdc42
1Graduate School of Natural Science and Technology; 2Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa, Japan; and 3Department of Biochemistry, Kagawa University School of Medicine, Miki, Kagawa, Japan
*To whom correspondence should be addressed. Tel: +81-76-234-4424, Fax: +81-76-234-4480, E-mail: shira{at}kenroku.kanazawa-u.ac.jp
Received May 29, 2008; Accepted October 16, 2008
| Abstract |
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The production of N-acylethanolamine (NAE) is enhanced during inflammation. NAE is synthesized from phosphatidylethanolamine with N-acylphosphatidylethanolamine (NAPE) as a precursor. The amount of NAPE at the site of inflammation exceeds that of NAE. This evokes the possibility that NAPE possesses a biological function, as does NAE. We here examined if N-palmitoylphosphatidylethanolamine (NPPE), a precursor of N-palmitoylethanolamine, modulates the state of inflammation. We found that the level of the phagocytosis of latex beads, Staphylococcus aureus, Escherichia coli, or apoptotic cells by mouse peritoneal macrophages or J774A.1 macrophages was reduced in the presence of liposomes containing NPPE, while that of dextran remained unaffected. This action of NPPE seemed to be due to the inhibition of the activation of Rac1 and Cdc42 in macrophages. These results suggested that NAPE is bioactive lipid acting toward the termination of inflammation.
Key Words: N-acylphosphatidylethanolamine, lipid mediator, macrophage, phagocytosis, Rho GTPase
Abbreviations: NAE, N-acylethanolamine; NAPE, N-acylphosphatidylethanolamine; NPE, N-palmitoylethanolamine; NPPE, N-palmitoylphosphatidylethanolamine; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PS, phosphatidylserine
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