
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
Author(s) -
CAMUSSI Giovanni,
TETTA Ciro,
BUSSOLINO Federico,
METAFORA Salvatore,
PELUSO Gianfranco,
ESPOSITO Carla,
PORTA Raffaele
Publication year - 1990
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1111/j.1432-1033.1990.tb19251.x
Subject(s) - platelet activating factor , phospholipase a2 , arachidonic acid , prostacyclin , phosphocholine , acetylation , seminal vesicle , phospholipase , chemistry , lipid signaling , biology , endocrinology , medicine , biochemistry , phospholipid , enzyme , phosphatidylcholine , prostate , cancer , membrane , gene
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 A 2 , 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 A 2 , that also results in the inhibition of arachidonic acid and prostacyclin release, and of acetyl‐CoA:lyso‐PAF acetyltransferase.