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A more recent version of this article appeared on January 1, 2003

Papers In Press, published online ahead of print October 1, 2002
J. Lipid Res., doi:10.1194/jlr.M200298-JLR200
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Submitted on July 29, 2002
Revised on September 3, 2002
Accepted on September 17, 2002

Brain lipid metabolism in the cytosolic phospholipase A2 knockout mouse

Thad A. Rosenberger, Nelly E. Villacreses, Miguel A. Contreras, Joseph V. Bonventre, and Stanley I. Rapoport

BPMS/NIA, National Institutes of Health, Bethesda, MD 20892

Corresponding Author: plsetn{at}mail.nih.gov

We examined brain phospholipid metabolism in mice in which the cytosolic phospholipase A2 (cPLA2, Type IV, 85 kDa) was knocked out (cPLA2(-/-) mice). Compared with controls, these mice demonstrated altered brain concentrations of several phospholipids, reduced esterified linoleate, arachidonate and docosahexaenoate in choline glycerophospholipid, and reduced esterified arachidonate in phosphatidylinositol. Unanesthetized cPLA2(-/-) mice had reduced rates of incorporation of unlabeled arachidonate from plasma and from the brain arachidonoyl-CoA pool into ethanolamine glycerophospholipid and choline glycerophospholipid, but elevated rates into phosphatidylinositol. These differences corresponded to altered turnover and metabolic loss of esterified brain arachidonate. These results suggests that cPLA2 is necessary to maintain normal brain concentrations of phospholipids and of their esterified polyunsaturated fatty acids. Reduced esterified arachidonate and docosahexaenoate may account for the resistance of the cPLA2(-/-) mouse to middle cerebral artery occlusion, and should influence membrane fluidity, neuroinflammation, signal transduction and other brain processes.


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