Ethanol differentially affects metabolic and mitotic processes in chick embryonic cells.
Ethanol differentially affects metabolic and mitotic processes in chick embryonic cells.
复制标题
乙醇对鸡胚胎细胞的代谢和有丝分裂过程有不同的影响。
DOI：
10.1111/j.1530-0277.1997.tb03791.x
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Pennington,SN
中科院分区：
文献类型：
--
作者：
ShibleyJr,IA;Carver,FM;Pennington,SN
我们的实验室一直在研究乙醇诱导的生长抑制在发育中的胚胎中发生的机制，我们的研究重点是破坏细胞信号通路。前人在乙醇诱导的信号系统中调节omithine脱羧酶活性的工作表明，含有蛋白激酶A、蛋白激酶C(PKC)和胰岛素依赖的酪氨酸激酶的信号通路对鸡胚胎细胞中omithine脱羧酶的控制是重要的。在这里，我们报告了乙醇对葡萄糖摄取和胸腺嘧啶核苷摄取的调节作用，这些都是通过这些相同的激酶途径实现的。葡萄糖摄取的显著增加与车辆和乙醇暴露的细胞中PKC的下调有关，其中乙醇暴露的细胞中的增加幅度更大。胸腺嘧啶核苷摄取的增加与所有三种激酶的激活以及PKC的下调有关。由于以前对信号通路的研究一直在寻找胰岛素信号通路的变化，所以本文的工作主要集中在涉及蛋白激酶A和PKC的信号通路上。乙醇处理使cAMP水平升高，但增加幅度相对较小。对乙醇诱导的PKC活性变化的分析表明，乙醇处理的细胞中PKC活性显著受到抑制，这表明总的来说，乙醇处理主要通过下调PKC来影响胚胎细胞葡萄糖摄取的调节。
Our laboratory has been investigating the mechanisms by which ethanol‐induced growth inhibition occurs in a developing embryo, and our studies have focused on disruption of cellular signaling pathways. Previous work on ethanol‐induced changes in signaling systems that regulate omithine decarboxylase activity indicated that the pathways containing protein kinase A, protein kinase C (PKC), and insulin‐dependent tyrosine kinase were important for the control of omithine decarboxylase in chick embryonic cells. Herein, we report ethanol's effect on the regulation of glucose uptake and thymidine uptake by these same kinase pathways. A pronounced increase in glucose uptake was associated with PKC downregulation in both vehicle‐ and ethanol‐exposed cells, with the larger increase occurring in ethanol‐exposed cells. An increase in thymidine uptake was associated with an activation of all three kinases, as well as with downregulation of PKC. Because previous work on signaling pathways has looked for changes in the insulin signaling pathway, the work herein focuses on the signaling pathways involving protein kinase A and PKC. cAMP levels were increased by ethanol treatment, but the increase was relatively small. Analysis of changes in PKC activity induced by ethanol exposure showed a significant suppression of PKC activity in the ethanol‐treated cells and suggested that, overall, ethanol treatment affects the regulation of glucose uptake in embryonic cells predominantly by PKC downregulation.