Transcellular metabolism of arachidonic acid: increased platelet thromboxane generation in the presence of activated polymorphonuclear leukocytes.
Transcellular metabolism of arachidonic acid: increased platelet thromboxane generation in the presence of activated polymorphonuclear leukocytes.
复制标题
花生四烯酸的跨细胞代谢:在活化的多形核白细胞存在下,血小板血栓素的产生增加。
作者:
N. Maugeri;V. Evangelista;P. Piccardoni;G. Dell'elba;A. Celardo;G. Gaetano;C. Cerletti
Human polymorphonuclear leukocytes (PMN) activated by n-formyl-methionyl-leucyl-phenylalanine (fMLP), in the presence of cytochalasin B, are able to induce activation of coincubated autologous platelets "via" cathepsin G released from the azurophilic granules. However, thromboxane (Tx) B2 production in this system cannot be completely explained by cathepsin G-stimulated platelet arachidonate metabolism. Indeed, the amount of TxB2 found in supernatants of platelet/PMN suspensions challenged with 1 mumol/L fMLP was twofold to fourfold higher than that measured when platelets were stimulated by supernatants from fMLP-activated PMN. In the present report, we analyzed the possibility that PMN-induced TxB2 production in this system is the result of transcellular metabolism of arachidonic acid (AA) between fMLP-activated PMN and cathepsin G-stimulated platelets. 3H-AA-labeled PMN were used to test if a transfer of AA or metabolite(s) occur from PMN to platelets. Our results showed that: (1) 3H-TxB2 and 3H-12-HHT are synthesized when 3H-AA-labeled PMN are activated mixed to unlabeled platelets; (2) total radioactivity released by fMLP-stimulated PMN is increased in the presence of platelets, whereas the membrane content of unesterified 3H-AA is reduced; (3) platelet cyclooxygenase inhibition completely prevents 3H-TxB2 synthesis; and (4) inhibition of cathepsin G-induced platelet activation with the antiprotease eglin C blocks the formation of 3H-TxB2. These data show that in the experimental system used, platelets use PMN-derived unmetabolized AA to synthesize TxB2.
登录
查看更多内容
影响因子:
15.9
作者:
SERHAN, CN;SHEPPARD, KA
通讯作者:
SHEPPARD, KA
DOI:
--
发表时间:
1988
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
Marcus,AJ;Safier,LB;Ullman,HL;Islam,N;Broekman,MJ;Falck,JR;Fischer,S;vonSchacky,C
通讯作者:
vonSchacky,C
DOI:
--
发表时间:
1984
期刊:
Clinical physiology and biochemistry
影响因子:
--
作者:
Marcus,AJ;Broekman,MJ;Safier,LB;Ullman,HL;Islam,N;Serhan,CN;Weissmann,G
通讯作者:
Weissmann,G
DOI:
10.1016/s0021-9258(19)57375-6
发表时间:
1988-01
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
Jacques A. MacloufS;R. C. Murphy
通讯作者:
Jacques A. MacloufS;R. C. Murphy
DOI:
--
发表时间:
1981
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
Walsh,CE;Waite,BM;Thomas,MJ;DeChatelet,LR
通讯作者:
DeChatelet,LR