Studies on the platelet-activating factor interaction with protein kinase C in human neutrophils.
Platelet-activating factor (PAF) stimulated neutrophils to translocate cytosolic protein kinase C (PKC) to plasmalemma by a Ca(2+)-transient-independent mechanism. Arachidonic acid had these same effects but unlike PAF acted independently, not only of Ca2+ transients but also of other cell Ca2+ pools. The fatty acid (which is released by PAF-challenged cells) may mediate PKC movements and thereby contribute to the many Ca(2+)-independent bioactions of PAF.
O'Flaherty
J T
JT
Department of Medicine, Wake Forest University Medical Center, Winston Salem, NC 27103.
D016718:Arachidonic Acid / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002413:Cations, Divalent; D002478:Cells, Cultured; D006801:Humans; D009504:Neutrophils / Q000187:drug effects / Q000201:enzymology*; D010972:Platelet Activating Factor / Q000494:pharmacology*; D011493:Protein Kinase C / Q000378:metabolism*
D002413:Cations, Divalent; D010972:Platelet Activating Factor; D016718:Arachidonic Acid; D011493:Protein Kinase C; D002118:Calcium