Resident mouse peritoneal macrophages synthesized and released prostaglandins (PGs) when challenged with 12-O-tetradecanoylphorbol 13-acetate (TPA) or 1,2-dioctanoyl-sn-glycerol (DiC8). Both stimuli were found to activate Ca2+/phospholipid-dependent protein kinase C (PKC). 1-(5-Isoquinolinesulphonyl)-2-methylpiperazine (‘H-7’) and D-sphingosine, known to inhibit PKC by different mechanisms, were able to decrease the PKC activity of macrophages in a dose-dependent manner. Addition of either PKC inhibitor decreased PG synthesis and also the release of arachidonic acid (AA) from phospholipids induced by TPA or DiC8. Simultaneously TPA or DiC8 also decreased incorporation of free AA into membrane phospholipids of macrophages. AA incorporation could be restored, however, by pretreatment with the PKC inhibitors. Our results demonstrate an involvement of PKC in the regulation of PG synthesis in mouse peritoneal macrophages and provide further evidence that reacylation of released fatty acids may be an important regulatory step.
Research Article|June 01 1989
Regulation of prostaglandin synthesis by protein kinase C in mouse peritoneal macrophages
H J Pfannkuche;
1*Division of Molecular Pharmacology, Department of Pharmacology and Toxicology, Medical School Hannover, D-3000 Hannover 61, Federal Republic of Germany
†Department of Immunology, Philipps University Marburg, D-3550 Marburg, Federal Republic of Germany
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Biochem J (1989) 260 (2): 471-478.
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H J Pfannkuche, V Kaever, D Gemsa, K Resch; Regulation of prostaglandin synthesis by protein kinase C in mouse peritoneal macrophages. Biochem J 1 June 1989; 260 (2): 471–478. doi: https://doi.org/10.1042/bj2600471
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