Department of Pharmacology, School of Medicine, Emory University, Atlanta, GA 30322, USA.
Neurotoxicology. 2011 Oct;32(5):563-6. doi: 10.1016/j.neuro.2011.05.019. Epub 2011 Jun 29.
Various isoforms of myocyte enhancer factor-2 (MEF2) constitute a group of nuclear proteins found to play important roles in increasing types of cells. In neurons, MEF2s are required to regulate neuronal development, synaptic plasticity, as well as survival. MEF2s promote the survival of several types of neurons under different conditions. In cellular models, negative regulation of MEF2s by stress and toxic signals contributes to neuronal death. In contrast, enhancing MEF2 activity not only protects cultured primary neurons from death in vitro but also attenuates the loss of dopaminergic neurons in substantia nigra pars compacta in a 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease. In this work, the mechanisms of regulation of MEF2 function by several well-known neurotoxins and their implications in various neurodegenerative diseases are reviewed.
肌细胞增强因子 2（MEF2）的各种异构体是一组核蛋白，被发现对多种细胞的增殖具有重要作用。在神经元中，MEF2 对于调节神经元发育、突触可塑性以及存活都是必需的。MEF2 可以促进多种神经元在不同条件下的存活。在细胞模型中，应激和毒性信号对 MEF2 的负向调节导致神经元死亡。相反，增强 MEF2 的活性不仅可以保护体外培养的原代神经元免于死亡，而且还可以减轻帕金森病 1-甲基-4-苯基-1,2,3,6-四氢吡啶模型中小脑黑质致密部多巴胺能神经元的丢失。在这项工作中，综述了几种已知神经毒素调节 MEF2 功能的机制及其在各种神经退行性疾病中的意义。
