Tumor necrosis factor stimulates human neutrophils to release leukotriene B4 and platelet-activating factor. Induction of phospholipase A2 and acetyl-CoA: 1-alkyl-sn-glycero-3-phosphocholine O2-acetyltransferase activity and inhibition by antiproteinase

G. Camussi, C. Tetta, F. Bussolino, C. Baglioni

Research output: Contribution to journalArticlepeer-review

Abstract

Tumor necrosis factor stimulates polymorphonuclearneutrophils to synthesize leukotriene B4 and platelet-activating factor (PAF), but α1-proteinase inhibitor and α1-antichymotrypsin block this response. However, proteinases such as elastase and cathepsin G induce preferentially synthesis of PAF. An acetyltransferase required, together with phospholipase A2, in the remodeling pathway of PAF synthesis is activated in polymorphonuclearneutrophils stimulated by tumor necrosis factor and elastase. In contrast, 1-oleyl-2-acetyl-glycerol, a protein kinase C activator, promotes PAF formation by the de novo biosynthetic pathway without activating the acetyltransferase. Staurosporine, an inhibitor of protein kinase C, blocks PAF production apparently by inhibiting phospholipase A2. This suggests that diacylglycerols are involved in activating both pathway of PAF synthesis.

Original languageEnglish
Pages (from-to)661-666
Number of pages6
JournalEuropean Journal of Biochemistry
Volume182
Issue number3
Publication statusPublished - 1989

ASJC Scopus subject areas

  • Biochemistry

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