ROLE OF KINASES AND G-PROTEINS ON ARACHIDONATE RELEASE INDUCED BY ZYMOSAN IN MOUSE PERITONEAL-MACROPHAGES

The present study investigated the role of kinases and G-proteins in a rachidonic acid (AA) mobilization by resident mouse peritoneal macroph ages in response to phagocytosis of opsonized zymosan. Stimulation of resident murine peritoneal macrophages with opsonized zymosan caused a n increase in [H-3] arachidonic acid release. This increase was dose-d ependent and was not accompanied by de novo synthesis of proteins. Nei ther staurosporine, a protein kinase C inhibitor, nor genistein, a tyr osine kinase inhibitor, had any effect on [H-3] AA mobilization, altho ugh trifluoperazine significantly inhibited AA release. The involvemen t of G proteins and phospholipase C (PLC) in the regulation of arachid onic acid release induced by opsonized zymosan was also examined in mo use peritoneal macrophages. Prior treatment of cells with pertussis to xin induced a partial decrease in AA mobilization. However, neomycin o r aspirin, at doses that inhibit inositol phosphate formation (PLC act ivity), did not decrease [H-3] AA mobilization by PLA(2). We proposed that the AA release by peritoneal macrophages in response to opsonized zymosan phagocytosis could be due to the participation of enzymes oth er than PLC and PKC, or proteins other than G proteins. Copyright (C) 1996 Elsevier Science Ltd.