Arachidonic acid mobilization in platelets: the possible role of protein kinase C and G-proteins.
A major route for the release of arachidonic acid from platelet phospholipids appears to be catalyzed by a phospholipase A2 that can be stimulated by a rise of cytosolic Ca2+. This paper discusses certain other mechanisms for regulation of this process. Release of arachidonic acid by calcium ionophores is potentiated by pretreatment with stimulators of protein kinase C; e.g. diglyceride, phorbol esters and the terpene diester mezerein. This effect appears to be coincident with phosphorylation of a certain group of proteins (not 47 KDa protein), and is sensitive to depletion of ATP, activation of Ca2+ dependent phosphatase, and the kinase C inhibitor H-7, but is unaffected by Na+/H+ exchange inhibitors. Recent results in other cell types strongly indicate that phospholipase A2 is also directly under control of certain GTP-binding proteins.
Feinstein
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MB
Department of Pharmacology, University of Connecticut Health Center, Farmington 06032.
Halenda
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SP
D017302:Annexins; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000097:blood*; D001792:Blood Platelets / Q000378:metabolism*; D001798:Blood Proteins / Q000378:metabolism; D002118:Calcium / Q000502:physiology; D002352:Carrier Proteins / Q000502:physiology; D004789:Enzyme Activation; D019204:GTP-Binding Proteins / Q000502:physiology*; D006023:Glycoproteins / Q000502:physiology; D006801:Humans; D010766:Phosphorylation; D011493:Protein Kinase C / Q000502:physiology*; D017923:Sodium-Hydrogen Exchangers
D017302:Annexins; D001095:Arachidonic Acids; D001798:Blood Proteins; D002352:Carrier Proteins; D006023:Glycoproteins; D017923:Sodium-Hydrogen Exchangers; D016718:Arachidonic Acid; D011493:Protein Kinase C; D019204:GTP-Binding Proteins; D002118:Calcium