乙酰胆碱酯酶多方面促进细胞凋亡

Debbra Y. Knorr, D. Demirbas, R. Heinrich
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引用次数: 0

摘要

乙酰胆碱酯酶(AChE)的表达升高是脊椎动物和无脊椎动物中凋亡细胞的共同特征。虽然乙酰胆碱酯酶水平升高使细胞对凋亡刺激敏感,但其缺乏或药理学失活会干扰凋亡细胞的死亡。乙酰胆碱酯酶可能作为凋亡分子机制的一个组成部分直接发挥其促凋亡功能,也可能通过限制非凋亡条件下促进细胞存活的受体配体和结构结合伙伴的可用性间接发挥其促凋亡功能。乙酰胆碱酯酶促进凋亡小体的形成,并在细胞核积累后降解DNA。乙酰胆碱的酯酶活性限制了乙酰胆碱作为配体用于细胞膜上烟碱和毒蕈碱乙酰胆碱受体和线粒体烟碱乙酰胆碱受体的可用性,而这些受体通常支持重要的生理状态。对昆虫的研究表明,细胞因子激活的细胞保护途径可能抑制凋亡条件下乙酰胆碱酯酶的过度表达,从而防止凋亡细胞死亡。我们概述了各种生物和细胞类型的研究,总结了乙酰胆碱酯酶通过多种机制对细胞凋亡进程的贡献。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Multifaceted promotion of apoptosis by acetylcholinesterase
Elevated expression of acetylcholinesterase (AChE) is a common characteristic of apoptotic cells in both invertebrate and vertebrate species. While increased levels of acetylcholinesterase sensitize cells to apoptogenic stimuli, its absence or pharmacological inactivation interferes with apoptotic cell death. acetylcholinesterase may exert its pro-apoptotic function directly as an integral component of the apoptotic molecular machinery or indirectly by limiting the availability of receptor ligands and structural binding partners that promote cell survival under non-apoptogenic conditions. acetylcholinesterase promotes formation of the apoptosome and degrades DNA after nuclear accumulation. Its esterase activity limits the availability of acetylcholine as ligand for cell membrane-located nicotinic and muscarinic ACh-receptors and mitochondrial nicotinic ACh-receptors that normally support vital physiological states. Studies on insects suggest, that cytokine-activated cell-protective pathways may suppress acetylcholinesterase overexpression under apoptogenic conditions to prevent apoptotic cell death. We provide an overview of studies on various organisms and cell types that summarizes the contribution of acetylcholinesterase to the progress of apoptosis via multiple mechanisms.
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