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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >Ethanol blocks both basic fibroblast growth factor- and carbachol-mediated neuroepithelial cell expansion with differential effects on carbachol-activated signaling pathways.
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Ethanol blocks both basic fibroblast growth factor- and carbachol-mediated neuroepithelial cell expansion with differential effects on carbachol-activated signaling pathways.

机译：乙醇会阻断碱性成纤维细胞生长因子和卡巴胆碱介导的神经上皮细胞的扩张，并对卡巴胆碱激活的信号通路产生不同的影响。

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摘要

We have expanded neuroepithelial cells dissociated from the embryonic rat telencephalon in serum-free defined medium containing basic fibroblast growth factor (bFGF) in order to generate a model neuroepithelium to study the interaction of ethanol with both growth factor- and transmitter-stimulated proliferation. Ethanol blocked proliferation stimulated by bFGF and by carbachol, an agonist at muscarinic acetylcholine receptors, in a dose-dependent manner. In addition, ethanol attenuated autonomous expansion of neuroepithelial cells occurring following withdrawal of bFGF. The latter effect was associated with an increase in the number of apoptotic cells identified by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling labeling. We studied the effects of ethanol on carbachol-stimulated signaling pathways critical to its proliferative effects. Ethanol significantly reduced carbachol-stimulated Ca(2+) signaling, as well as Erk1/Erk2, Akt and cyclic AMP-response element-binding phosphorylations in a dose-dependent manner. Comparison of the potency of ethanol in attenuating carbachol-stimulated proliferation and signal transduction showed that mitogen-activated protein kinase phosphorylation was less sensitive to ethanol than the other parameters. The results indicate that ethanol's suppression of proliferation induced by carbachol in this model neuroepithelium likely involves multiple signaling pathways. These effects in vitro may help to explain the devastating effects of prenatal ethanol exposure in vivo, which contribute to the fetal alcohol syndrome.
机译：我们已经在含有碱性成纤维细胞生长因子（bFGF）的无血清明确培养基中扩增了与胚胎大鼠端脑分离的神经上皮细胞，以产生模型神经上皮，以研究乙醇与生长因子和递质刺激的增殖的相互作用。乙醇以剂量依赖性方式阻断bFGF和毒蕈碱乙酰胆碱受体激动剂卡巴胆碱刺激的增殖。另外，乙醇减弱了bFGF退出后发生的神经上皮细胞的自主扩增。后一种效应与通过末端脱氧核苷酸转移酶介导的dUTP缺口末端标记标记鉴定的凋亡细胞数量增加有关。我们研究了乙醇对卡巴胆碱刺激的对其增殖作用至关重要的信号通路的影响。乙醇以剂量依赖的方式显着降低了卡巴胆碱刺激的Ca（2+）信号传导，以及Erk1 / Erk2，Akt和环AMP响应元素结合的磷酸化。乙醇在减弱卡巴胆碱刺激的增殖和信号转导中的效力的比较显示，有丝分裂原激活的蛋白激酶磷酸化对乙醇的敏感性低于其他参数。结果表明在该模型神经上皮中乙醇对卡巴胆碱诱导的增殖的抑制可能涉及多个信号通路。体外的这些作用可能有助于解释体内产前乙醇暴露的毁灭性作用，其导致胎儿酒精综合症。

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