Tyagi S R, Olson S C, Burnham D N, Lambeth J D
Department of Biochemistry, Emory University Medical School, Atlanta, Georgia 30322.
J Biol Chem. 1991 Feb 25;266(6):3498-504.
Agents which elevate cellular cAMP (prostaglandin E2, theophylline, and forskolin) or mimic cAMP action (dibutyryl cAMP) are known to inhibit human neutrophil activation (superoxide generation and secretion) by receptor-linked agonists such as formyl-methionyl-leucyl-phenylalanine (fMLP). Herein, we show that these agents also markedly inhibit fMLP-stimulated diradylglycerol generation (assayed by mass methods). The magnitude of inhibition correlated with the ability of a given agent or combination of agents to elevate cAMP. Both 1,2-diacylglycerol and 1-O-alkyl,2-acyl glycerol generation were affected. Effects on the latter species, as well as a lack of effect on fMLP-stimulated inositol phosphate release, implied that cAMP affected diradylglycerol generation from a source other than phospholipase C-dependent phosphoinositide hydrolysis, since phosphatidylinositols do not contain appreciable quantities of the 1-O-alkyl linkage. In cells in which the phosphatidylcholine pool was prelabeled using 1-O-[3H]octadecyl-2-lyso-sn-glycero-3-phosphocholine, prostaglandin E2 plus theophylline inhibited the fMLP-activated rapid generation of [3H]phosphatidic acid and its subsequent conversion to [3H]diradylglycerol, implying an effect at the level of phospholipase D. In the presence of ethanol, the fMLP-activated transphosphatidylation of [3H]phosphatidylcholine to generate [3H]phosphatidylethanol (a phospholipase D-dependent reaction) was also markedly inhibited. In contrast, when phorbol 12-myristate 13-acetate was used to activate cells, cAMP-related agents had no effect on phospholipase D activity, diradylglycerol generation, or superoxide generation. The data indicate an inhibitory effect of cyclic AMP on receptor-mediated phospholipase D activation at a site proximal to phospholipase D (e.g., the receptor or G protein). These studies provide a new example of "cross-talk" among signal transduction systems.
已知能提高细胞内环磷酸腺苷(cAMP)水平的物质(前列腺素E2、茶碱和福斯可林)或模拟cAMP作用的物质(二丁酰cAMP)可抑制受体介导的人类中性粒细胞激活(超氧化物生成和分泌),如甲酰甲硫氨酰亮氨酰苯丙氨酸(fMLP)。在此,我们表明这些物质也能显著抑制fMLP刺激的二酰基甘油生成(通过质谱法检测)。抑制程度与特定物质或物质组合提高cAMP的能力相关。1,2 - 二酰基甘油和1 - O - 烷基 - 2 - 酰基甘油的生成均受到影响。对后一种物质的影响以及对fMLP刺激的肌醇磷酸释放缺乏影响,意味着cAMP影响二酰基甘油的生成并非源于磷脂酶C依赖性磷酸肌醇水解,因为磷脂酰肌醇不含大量的1 - O - 烷基连接。在用1 - O - [3H]十八烷基 - 2 - 溶血 - sn - 甘油 - 3 - 磷酸胆碱预标记磷脂酰胆碱池的细胞中,前列腺素E2加茶碱抑制了fMLP激活的[3H]磷脂酸的快速生成及其随后向[3H]二酰基甘油的转化,这意味着在磷脂酶D水平上有作用。在乙醇存在的情况下,fMLP激活的[3H]磷脂酰胆碱转磷脂酰基作用生成[3H]磷脂酰乙醇(一种磷脂酶D依赖性反应)也受到显著抑制。相反,当使用佛波醇12 - 肉豆蔻酸酯13 - 乙酸酯激活细胞时,cAMP相关物质对磷脂酶D活性、二酰基甘油生成或超氧化物生成均无影响。数据表明环磷酸腺苷在靠近磷脂酶D的位点(如受体或G蛋白)对受体介导的磷脂酶D激活有抑制作用。这些研究提供了信号转导系统之间“串扰”的一个新例子。