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Am J Physiol Cell Physiol 255: C589-C594, 1988;
0363-6143/88 $5.00
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AJP - Cell Physiology, Vol 255, Issue 5 C589-C594, Copyright © 1988 by American Physiological Society

ARTICLES

Diacylglycerol kinase inhibitor R59022 and stimulated neutrophil responses

J. L. Mege, W. Tao, T. F. Molski, J. Gomez-Cambronero, C. K. Huang, E. L. Becker and R. I. Sha'afi
Department of Physiology, University of Connecticut Health Center, Farmington 06032.

The generation of phosphatidic acid in neutrophils stimulated by the chemotactic factor formylmethionyl-leucyl-phenylalanine (fMet-Leu-Phe) is inhibited by the diacylglycerol kinase inhibitor R59022. Superoxide generation produced by fMet-Leu-Phe, leukotriene B4, platelet-activating factor, or phorbol 12-myristate 13-acetate can be greatly increased in neutrophils pretreated with R59022. The potentiation occurs in the presence or absence of cytochalasin B and is evident in the absence of extracellular calcium. In addition, where the superoxide generated by fMet-Leu-Phe is not inhibited by the protein kinase C inhibitor 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), the increase by R59022 is diminished by this compound. Unlike cytochalasin B, R59022 does not affect the increase in cytoskeletal actin produced by fMet-Leu-Phe or platelet-activating factor nor does it decrease the basal level. Furthermore, the basal intracellular concentration of free calcium, but not the rise produced by fMet-Leu-Phe or platelet-activating factor, is elevated by R59022. The data presented here suggest that the potentiation by R59022 of the oxidative burst is most likely mediated through protein kinase C.


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[Abstract] [Full Text] [PDF]


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