Synergy between phorbol esters, 1-oleyl-2-acetylglycerol, urushiol, and calcium ionophore in eliciting aggregation of marine sponge cells.

Synergy between phorbol esters, 1-oleyl-2-acetylglycerol, urushiol, and calcium ionophore in eliciting aggregation of marine sponge cells.
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佛波酯、1-油酰基-2-乙酰甘油、漆酚和钙离子载体之间的协同作用引起海洋海绵细胞的聚集。

DOI:
10.1073/pnas.83.9.2914
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发表时间:
1986
影响因子:
11.1
通讯作者:
Dunham,P
Dunham,P
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Weissmann,G;Azaroff,L;Davidson,S;Dunham,P

文献摘要

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海绵细胞(Microciona prolifera)的聚集类似于高等生物的刺激-反应偶联,其中蛋白激酶C的激活和细胞内Ca的运动提供双信号。我们现在报告,蛋白激酶C(佛波醇酯)和离子霉素的激活剂协同作用,聚集海绵细胞。令人惊讶的是--由于细胞外Ca是物种特异性聚集因子的完整性所必需的--协同聚集在完全不添加细胞外Ca(2.5-20 mM EDTA)的情况下进行。佛波醇酯和相关化合物的活性顺序是它们对蛋白激酶C的作用顺序(佛波醇肉豆蔻酸酯乙酸酯、佛波醇二丁酸酯大于佛波醇二乙酸酯,远大于佛波醇、4 α-佛波醇)。1-油酰基,2-乙酰基甘油是蛋白激酶C的合成激活剂,也显示出与离子霉素的协同作用。佛波酯和1-油基,2-乙酰基甘油协同作用与离子霉素释放膜钙检测减少荧光金霉素在预标记的细胞。此外,漆酚,毒葛的毒性原则,但不是十五烷基儿茶酚,其惰性类似物,显示协同作用与离子霉素。钙咪达唑鎓(10 μ M)、吡罗昔康(20-100 μ M)和百日咳毒素(20 μ g/ml)可抑制协同聚集。这些数据不仅证实了海绵细胞聚集遵循高等生物细胞中刺激-反应偶联的一般顺序,而且还支持在这种最古老的多细胞生物中,细胞内Ca的动员和蛋白激酶C的激活提供了在没有细胞外Ca的情况下细胞激活的双信号的假设。
Aggregation of marine sponge cells (Microciona prolifera) resembles stimulus-response coupling of higher organisms in which activation of protein kinase C and movements of intracellular Ca provide twin signals. We now report that activators of protein kinase C (phorbol esters) and ionomycin act synergistically to aggregate sponge cells. Surprisingly--since extracellular Ca is required for integrity of the species-specific aggregation factor--synergistic aggregation proceeded in the complete absence of added extracellular Ca (2.5-20 mM EDTA). The order of activity of phorbol esters and related compounds was that of their effect on protein kinase C (phorbol myristate acetate, phorbol dibutyrate greater than phorbol diacetate much greater than phorbol, 4 alpha-phorbol). 1-Oleyl, 2-acetylglycerol a synthetic activator of protein kinase C, also showed synergy with ionomycin. Phorbol esters and 1-oleyl, 2-acetylglycerol acted in synergy with ionomycin to liberate membrane Ca as detected by decreased fluorescence of chlortetracycline in prelabeled cells. Moreover, urushiol, the toxic principle of poison ivy, but not pentadecanylcatechol, its inert analogue, showed synergy with ionomycin. Synergistic aggregation was inhibited by calmidazolium (10 microM), piroxicam (20-100 microM), and pertussis toxin (20 micrograms/ml). The data not only confirm that marine sponge cell aggregation follows the general sequence of stimulus-response coupling in the cells of higher organisms but also support, in this most ancient of multicellular creatures, the hypothesis that mobilization of intracellular Ca and activation of protein kinase C provide the twin signals for cell activation in the absence of added extracellular Ca.