Platele‐activating factor (PAF), a 1‐O‐alkyl‐2‐acetyl‐sn‐glycero‐3‐phosphocholine, is a mediator of inflammation and endotoxic shock produced by a variety of stimulated cells. Since the main biosynthetic pathway of PAF involves acetylation of 1‐O‐alkyl‐sn‐glycero‐3‐phosphocholine (lyso‐PAF) generated from 1‐O‐alkyl‐2‐acyl‐sn‐glycero‐3‐phosphocholine by phospholipase A2, we suggest a general physiological role played by steroid‐induced anti‐(phospholipase A2) proteins in the modulation of PAF synthesis. The results of the present study support this hypothesis since an androgen‐induced anti‐inflammatory protein, SV‐IV, secreted from rat seminal vesicles, inhibits PAF synthesis in stimulated polymorphonuclear neutrophils, macrophages and endothelial cells. SV‐IV impairs PAF synthesis by inhibiting the activation of phospholipase A2, that also results in the inhibition of arachidonic acid and prostacyclin release, and of acetyl‐CoA:lyso‐PAF acetyltransferase. Copyright © 1990, Wiley Blackwell. All rights reserved

An anti-inflammatory protein secreted from the rat seminal vesicle epithelium inhibits the synthesis of platelet-activating factor and the release of arachidonic acid and prostacyclin

Peluso, Gianfranco;
1990-01-01

Abstract

Platele‐activating factor (PAF), a 1‐O‐alkyl‐2‐acetyl‐sn‐glycero‐3‐phosphocholine, is a mediator of inflammation and endotoxic shock produced by a variety of stimulated cells. Since the main biosynthetic pathway of PAF involves acetylation of 1‐O‐alkyl‐sn‐glycero‐3‐phosphocholine (lyso‐PAF) generated from 1‐O‐alkyl‐2‐acyl‐sn‐glycero‐3‐phosphocholine by phospholipase A2, we suggest a general physiological role played by steroid‐induced anti‐(phospholipase A2) proteins in the modulation of PAF synthesis. The results of the present study support this hypothesis since an androgen‐induced anti‐inflammatory protein, SV‐IV, secreted from rat seminal vesicles, inhibits PAF synthesis in stimulated polymorphonuclear neutrophils, macrophages and endothelial cells. SV‐IV impairs PAF synthesis by inhibiting the activation of phospholipase A2, that also results in the inhibition of arachidonic acid and prostacyclin release, and of acetyl‐CoA:lyso‐PAF acetyltransferase. Copyright © 1990, Wiley Blackwell. All rights reserved
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14245/4068
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