Huang C F, Cabot M C
W. Alton Jones Cell Science Center, Lake Placid, New York 12946.
J Biol Chem. 1990 Sep 5;265(25):14858-63.
The effect of the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), on phospholipid degradation was investigated in three cell lines of dissimilar origin, Madin-Darby canine kidney cells (MDCK), rat aorta smooth muscle cells (RASM), and bovine pulmonary artery endothelial cells (BPAE). In cells prelabeled with [3H]myristic acid, which is predominantly incorporated into phosphatidylcholine (PC), TPA treatment (80 nM) in the absence or presence of ethanol (2%) in the culture medium resulted in either the rapid generation of [3H]phosphatidate (PA) or the sustained accumulation of [3H]phosphatidylethanol (PEt), respectively. Increases in [3H]PA and [3H]PEt were paralleled by quantitative decreases in cellular [3H]PC radioactivity. TPA-induced [3H]PEt formation occurred in a similar fashion, irrespective of the presence of Ca2+ in the culture medium. The experiments demonstrate that TPA elicits PC degradation by phospholipase D (PLD) in cells of diverse origin. Data from further experiments revealed a complex relationship between TPA-induced [3H]PA and [3H]diacylglycerol (DG) generation in the three cell lines that was suggestive of dual pathways for the generation of [3H]DG. Experiments to discern the pathways for TPA-induced, PC-derived DG were conducted by comparing the variation of [3H]PA and [3H]DG formation in the absence and in the presence of increasing ethanol concentrations in the culture medium. With increasing amounts of ethanol, the formation of [3H]PA decreased at the expense of [3H]PEt formation, and depending upon the pathway operable, the amount of [3H]DG formed was either decreased, indicative of indirect formation of DG via PA phosphohydrolase, or not modified, indicative of DG formation by a direct phospholipase C (PLC) pathway. Increasing the concentration of ethanol in the medium blocked TPA-induced [3H]DG generation in MDCK cells in a concentration-dependent manner, while the formation of [3H]PEt increased at the expense of [3H]PA formation. In BPAE cells the presence of ethanol likewise reduced TPA-elicited formation of DG. Conversely, in two smooth muscle cell lines, RASM and A-10, ethanol was without influence on TPA-induced formation of [3H]DG, although [3H]PEt was generated at the expense of [3H]PA. In RASM cells prelabeled with [3H]choline, TPA induced the release to the medium of [3H]choline and [3H]phosphocholine, indicative of both PLD and PLC activation. These results show that TPA elicits DG formation from PC in MDCK cells predominantly by an indirect pathway, whereas in arterial smooth muscle cells DG is formed in part by the direct action of PLC.(ABSTRACT TRUNCATED AT 400 WORDS)
研究了肿瘤促进剂12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)对三种不同来源细胞系中磷脂降解的影响,这三种细胞系分别是马 - 达二氏犬肾细胞(MDCK)、大鼠主动脉平滑肌细胞(RASM)和牛肺动脉内皮细胞(BPAE)。在用[3H]肉豆蔻酸预标记的细胞中,[3H]肉豆蔻酸主要掺入磷脂酰胆碱(PC),在培养基中不存在或存在乙醇(2%)的情况下,TPA处理(80 nM)分别导致[3H]磷脂酸(PA)迅速生成或[3H]磷脂酰乙醇(PEt)持续积累。[3H]PA和[3H]PEt的增加与细胞中[3H]PC放射性的定量减少平行。无论培养基中是否存在Ca2+,TPA诱导的[3H]PEt形成方式相似。实验表明,TPA在不同来源的细胞中通过磷脂酶D(PLD)引发PC降解。进一步实验的数据揭示了三种细胞系中TPA诱导的[3H]PA和[3H]二酰甘油(DG)生成之间的复杂关系,这暗示了[3H]DG生成的双重途径。通过比较培养基中乙醇浓度增加时[3H]PA和[3H]DG形成的变化,进行了辨别TPA诱导的、源自PC的DG途径的实验。随着乙醇量增加以[3H]PEt形成增加为代价,[3H]PA形成减少,并且根据可操作的途径,形成的[3H]DG量要么减少,表明通过PA磷酸水解酶间接形成DG,要么不变,表明通过直接磷脂酶C(PLC)途径形成DG。增加培养基中乙醇浓度以浓度依赖方式阻断了TPA诱导的MDCK细胞中[3H]DG生成,而[3H]PEt形成增加以[3H]PA形成减少为代价。在BPAE细胞中,乙醇的存在同样减少了TPA诱导的DG形成。相反,在两种平滑肌细胞系RASM和A - 10中,乙醇对TPA诱导的[3H]DG形成没有影响,尽管以[3H]PA为代价生成了[3H]PEt。在用[3H]胆碱预标记的RASM细胞中,TPA诱导[3H]胆碱和[3H]磷酸胆碱释放到培养基中,表明PLD和PLC均被激活。这些结果表明,TPA在MDCK细胞中主要通过间接途径从PC引发DG形成,而在动脉平滑肌细胞中,DG部分通过PLC的直接作用形成。(摘要截短于400字)