Marin Raquel, Marrero-Alonso Jorge, Fernandez Cecilia, Cury Debora, Diaz Mario
Laboratory of Cellular Neurobiology, Department of Physiology, School of Medicine, La Laguna University, Tenerife, Spain.
Front Biosci (Elite Ed). 2012 Jan 1;4(4):1420-33. doi: 10.2741/471.
Estrogens exert a plethora of actions conducted to brain preservation and functioning. Some of these actions are initiated in lipid rafts, which are particular microstructures of the plasma membrane. Preservation of lipid raft structure in neurons is essential for signal transduction against different injuries, such as Alzheimer's disease (AD). These membrane structures appear to be disrupted as this neuropathology evolves, and that may largely contribute to dysfunction of raft resident proteins involved in intracellular signalling. This review includes a survey of some protein interactions that are involved in the structural maintenance and signal transduction mechanisms for neuronal survival against AD. Particularly relevant are the rapid mechanisms developed by estrogen to prevent neuronal death, through membrane estrogen receptors (mER) interactions with a voltage-dependent anion channel (VDAC) and other protein markers within neuronal lipid rafts. These interactions may have important consequences in estrogen mechanisms to achieve neuroprotection against amyloid beta (Abeta-induced toxicity).
雌激素发挥着大量作用,这些作用有助于大脑的保护和功能维持。其中一些作用始于脂筏,脂筏是质膜的特殊微观结构。神经元中脂筏结构的维持对于抵抗不同损伤(如阿尔茨海默病,AD)的信号转导至关重要。随着这种神经病理学的发展,这些膜结构似乎会遭到破坏,这可能在很大程度上导致参与细胞内信号传导的脂筏驻留蛋白功能失调。本综述包括对一些蛋白质相互作用的研究,这些相互作用参与了神经元抵抗AD存活的结构维持和信号转导机制。特别相关的是雌激素通过膜雌激素受体(mER)与神经元脂筏内的电压依赖性阴离子通道(VDAC)及其他蛋白质标志物相互作用而形成的快速机制,以防止神经元死亡。这些相互作用可能在雌激素实现针对β淀粉样蛋白(Aβ诱导毒性)的神经保护机制中产生重要影响。