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J. Biol. Chem., Vol. 276, Issue 27, 24743-24750, July 6, 2001

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Protein Kinases C Translocation Responses to Low Concentrations of Arachidonic Acid^*

Joseph T. O'Flaherty, Brad A. Chadwell, Mary W. Kearns^§, Susan Sergeant^§, and Larry W. Daniel

From the Departments of Internal Medicine and ^§ Biochemistry, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157

Arachidonic acid (AA) directly activates protein kinases C (PKC) and may thereby serve as a regulatory signal during cell stimulation. The effect, however, requires a 20 µM concentration of the fatty acid. We find that human polymorphonuclear neutrophils (PMN) equilibrated with a ligand for the diacylglycerol receptor on PKC, [³H]phorbol dibutyrate (PDB), increased binding of [³H]PDB within 15 s of exposure to 10-30 nM AA. Other unsaturated fatty acids, but not a saturated fatty acid, likewise stimulated PDB binding. These responses, similar to those caused by chemotactic factors, resulted from a rise in the number of diacylglycerol receptors that were plasma membrane-associated and therefore accessible to PDB. Unlike chemotactic factors, however, AA was fully active on cells overloaded with Ca²⁺ chelators. The major metabolites of AA made by PMN, leukotriene B₄ and 5-hydroxyicosatetraenoate, did not mimic AA, and an AA antimetabolite did not block responses to AA. AA also induced PMN to translocate cytosolic PKC, _II, and  to membranes. This response paralleled PDB binding with respect to dose requirements, time, Ca²⁺-independence, resistance to an AA antimetabolite, and induction by another unsaturated fatty acid but not by a saturated fatty acid. Finally, HEK 293 cells transfected with vectors encoding PKC_I or PKC fused to the reporter enhanced green fluorescent protein (EGFP) were studied. AA caused EGFP-PKC translocation from cytosol to plasma membrane at 0.5 µM, and EGFP-PKC translocation from cytosol to nuclear and, to a lesser extent, plasma membrane at as little as 30 nM. We conclude that AA induces PKC translocations to specific membrane targets at concentrations 2-4 orders of magnitude below those activating the enzymes. These responses, at least as they occur in PMN, do not require changes in cell Ca²⁺ or oxygenation of the fatty acid. AA seems more suited for signaling the movement than activation of PKC.

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