Long-term phorbol ester treatment dissociates phospholipase D activation from phosphoinositide hydrolysis and prostacyclin synthesis in endothelial cells stimulated with bradykinin.
Long-term phorbol ester treatment dissociates phospholipase D activation from phosphoinositide hydrolysis and prostacyclin synthesis in endothelial cells stimulated with bradykinin.
复制标题
长期佛波酯治疗可将磷脂酶 D 的激活与缓激肽刺激的内皮细胞中的磷酸肌醇水解和前列环素合成分离。
DOI：
10.1016/0006-291x(89)91072-3
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发表时间：
1989
影响因子：
3.1
通讯作者：
Wagner,JR
中科院分区：
文献类型：
--
作者：
Martin,TW;Feldman,DR;Goldstein,KE;Wagner,JR
用[3 H]胆碱或[3 H]肉豆蔻酸预先标记牛肺动脉内皮细胞(BPAEC)，选择性标记内源性磷脂酰胆碱。用三磷酸腺苷和缓激肽(BK)刺激BPAEC，经[~3H]胆碱标记的细胞的磷脂酶D(PLD)活性增加4倍，经[~H]肉豆蔻酸标记的细胞的[~3 H]磷脂酰乙醇量增加2~3倍。0.1Mphorbol 12-肉豆蔻酸13-醋酸酯(μM phorbol 12-Myriate 13-醋酸酯，PMA)处理BPAEC 22小时后，可完全抑制激动剂诱导的PLD激活，促进前列环素合成和[~3H]磷脂酰肌醇([~3H]Pins)水解率。因此，长期的PMA治疗将激动剂诱导的PLD激活与[~3H]Pins的水解分离，激动剂诱导的前列环素合成不依赖于PLD的激活。
Bovine pulmonary artery endothelial cells (BPAEC) were prelabeled with [3H]choline or [3H]myristic acid to selectively label endogenous phosphatidylcholine. BPAEC were stimulated with ATP and bradykinin (BK), and phospholipase D (PLD) activation was detected as a 4-fold increase in [3H]choline in cells prelabeled with [3H]choline or as a 2- to 3-fold increase in [3H]phosphatidylethanol in cells prelabeled with [3H]myristic acid and stimulated in the presence of ethanol. Pretreatment of BPAEC with 0.1 μM phorbol 12-myristate 13-acetate (PMA) for 22 hr completely inhibited agonist-induced PLD activation, whereas prostacyclin synthesis and [3H]phosphoinositide ([3H]PIns) hydrolysis were enhanced in pretreated cells. Long-term PMA treatment thus dissociates agonist-induced PLD activation from [3H]PIns hydrolysis, and agonist-induced prostacyclin synthesis is not dependent upon PLD activation.