补体因子C5a受体在NFL基因敲除小鼠的运动神经元中上调。
The complement factor C5a receptor is upregulated in NFL-/- mouse motor neurons.
作者信息
Humayun Saima, Gohar May, Volkening Kathryn, Moisse Katie, Leystra-Lantz Cheryl, Mepham Jennifer, McLean Jesse, Strong Michael J
机构信息
Department of Pathology, Schulich School of Medicine, University of Western Ontario, London, Canada.
出版信息
J Neuroimmunol. 2009 May 29;210(1-2):52-62. doi: 10.1016/j.jneuroim.2009.01.028. Epub 2009 Mar 16.
In NFL-/- mice, a model of motor neuron degeneration in ALS, degenerating spinal motor neurons express high levels of the receptor for the C5a anaphylatoxin (C5aR) early in the disease process. C5a is a potent in vitro neurotoxin for both Neuro2A and NGF-differentiated PC12 cells. While no interaction was observed between glutamate and C5a, both C5a and kainate upregulated the expression of activated C5aR. C5aR expression was increased in motor neurons in ALS. This data suggests that the early upregulation of C5aR may contribute to motor neuron damage that potentiates excitotoxicity in ALS.
在NFL基因敲除小鼠（一种肌萎缩侧索硬化症中运动神经元变性的模型）中，退化的脊髓运动神经元在疾病进程早期就高表达C5a过敏毒素受体（C5aR）。C5a对Neuro2A细胞和经神经生长因子（NGF）分化的PC12细胞而言，在体外是一种强效神经毒素。虽然未观察到谷氨酸与C5a之间存在相互作用，但C5a和海人酸均上调了活化型C5aR的表达。肌萎缩侧索硬化症患者运动神经元中的C5aR表达增加。该数据表明，C5aR的早期上调可能导致运动神经元损伤，从而增强肌萎缩侧索硬化症中的兴奋性毒性作用。
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