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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Ethanol enhances growth factor activation of mitogen-activated protein kinases by a protein kinase C-dependent mechanism.
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Ethanol enhances growth factor activation of mitogen-activated protein kinases by a protein kinase C-dependent mechanism.

机译：乙醇通过蛋白激酶C依赖性机制增强促分裂原活化蛋白激酶的生长因子激活。

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摘要

Excessive alcohol consumption alters neuronal growth and causes striking elongation of axons and dendrites in several brain regions. This could result from increased sensitivity to neurotrophic factors, since ethanol markedly enhances nerve growth factor (NGF)- and basic fibroblast growth factor (bFGF)-stimulated neurite outgrowth in the neural cell line PC12. The mechanism by which ethanol enhances growth factor responses was investigated by examining activation of mitogen-activated protein kinases (MAP kinases), a key event in growth factor signaling. Ethanol (100 mM) increased NGF- and bFGF-induced activation of MAP kinases. This increase, like ethanol-induced increases in neurite outgrowth, was prevented by down regulation of beta, delta, and epsilon protein kinase C (PKC) isozymes. Since chronic ethanol exposure specifically upregulates delta and epsilon PKC, these findings suggest that ethanol promotes neurite growth by enhancing growth factor signal transduction through a delta or epsilon PKC-regulated pathway.
机译：过量饮酒会改变神经元的生长，并在几个大脑区域引起轴突和树突的明显伸长。这可能是由于对神经营养因子的敏感性提高，因为乙醇显着增强了神经细胞系PC12中神经生长因子（NGF）和碱性成纤维细胞生长因子（bFGF）刺激的神经突生长。通过检查有丝分裂原激活的蛋白激酶（MAP激酶）的激活来研究乙醇增强生长因子应答的机制，这是生长因子信号传导中的关键事件。乙醇（100 mM）增加NGF和bFGF诱导的MAP激酶激活。像乙醇诱导的神经突增生一样，这种增加可以通过下调β，δ和ε蛋白激酶C（PKC）同工酶来防止。由于长期的乙醇暴露特别上调了δ和εPKC，因此这些发现表明，乙醇通过增强通过δ或εPKC调节途径的生长因子信号转导来促进神经突生长。

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