AN ANTIINFLAMMATORY PROTEIN SECRETED FROM THE RAT SEMINAL-VESICLE EPITHELIUM INHIBITS THE SYNTHESIS OF PLATELET-ACTIVATING FACTOR AND THE RELEASE OF ARACHIDONIC-ACID AND PROSTACYCLIN

被引:25
作者
CAMUSSI, G
TETTA, C
BUSSOLINO, F
METAFORA, S
PELUSO, G
ESPOSITO, C
PORTA, R
机构
[1] NAPLES UNIV,DIPARTIMENTO BIOCHIM & BIOFIS,I-80138 NAPLES,ITALY
[2] UNIV TURIN,DIPARTIMENTO GENET BIOL & CHIM CLIN,I-10124 TURIN,ITALY
[3] CNR,IST INT GENET & BIOFIS,NAPLES,ITALY
[4] CNR,IST BIOCHIM PROT & ENZIMOL,NAPLES,ITALY
来源
EUROPEAN JOURNAL OF BIOCHEMISTRY | 1990年 / 192卷 / 02期
关键词
D O I
10.1111/j.1432-1033.1990.tb19251.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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
引用
收藏
页码:481 / 485
页数:5
相关论文
共 33 条
[1]  
ABRESCIA P, 1985, J REPROD FERTIL, V73, P71
[2]  
BLIGH EG, 1959, CAN J BIOCHEM PHYS, V37, P911
[3]  
BRAQUET P, 1987, PHARMACOL REV, V39, P97
[4]   PLATELET-ACTIVATING-FACTOR AND CELLULAR IMMUNE-RESPONSES [J].
BRAQUET, P ;
ROLAPLESZCZYNSKI, M .
IMMUNOLOGY TODAY, 1987, 8 (11) :345-350
[5]  
BUSSOLINO F, 1988, J BIOL CHEM, V263, P11856
[6]  
BUSSOLINO F, 1986, J BIOL CHEM, V261, P6502
[7]   POTENTIAL ROLE OF PLATELET-ACTIVATING-FACTOR IN RENAL PATHOPHYSIOLOGY [J].
CAMUSSI, G .
KIDNEY INTERNATIONAL, 1986, 29 (02) :469-477
[8]   TUMOR NECROSIS FACTOR/CACHECTIN STIMULATES PERITONEAL-MACROPHAGES, POLYMORPHONUCLEAR NEUTROPHILS, AND VASCULAR ENDOTHELIAL-CELLS TO SYNTHESIZE AND RELEASE PLATELET-ACTIVATING-FACTOR [J].
CAMUSSI, G ;
BUSSOLINO, F ;
SALVIDIO, G ;
BAGLIONI, C .
JOURNAL OF EXPERIMENTAL MEDICINE, 1987, 166 (05) :1390-1404
[9]   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 [J].
CAMUSSI, G ;
TETTA, C ;
BUSSOLINO, F ;
BAGLIONI, C .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1989, 182 (03) :661-666
[10]   SYNTHESIS AND RELEASE OF PLATELET-ACTIVATING FACTOR IS INHIBITED BY PLASMA ALPHA-1-PROTEINASE INHIBITOR OR ALPHA-1-ANTICHYMOTRYPSIN AND IS STIMULATED BY PROTEINASES [J].
CAMUSSI, G ;
TETTA, C ;
BUSSOLINO, F ;
BAGLIONI, C .
JOURNAL OF EXPERIMENTAL MEDICINE, 1988, 168 (04) :1293-1306