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睫状神经营养因子过量产生会加速运动神经元变性(MND)小鼠症状的出现。

CNTF overproduction hastens onset of symptoms in motor neuron degeneration (mnd) mice.

作者信息

Winter C G, Saotome Y, Saotome I, Hirsh D

机构信息

Department of Biochemistry and Molecular Biophysics, Columbia University, New York, New York 10032, USA.

出版信息

J Neurobiol. 1996 Nov;31(3):370-8. doi: 10.1002/(SICI)1097-4695(199611)31:3<370::AID-NEU9>3.0.CO;2-7.

Abstract

Ciliary neurotrophic factor (CNTF) promotes the survival of motor neurons, in vitro and in vivo. Moreover, CNTF can block the degeneration of injured or diseased motor neurons in young rodents. Motor neuron degeneration (mnd) mutant mice display adult onset symptoms reflecting progressive motor debilitation and provide a model in which to test the hypothesis that CNTF can prevent the loss of these motor functions. We generated mnd mice that harbor a genomically integrated transgene, resulting in overexpression of the encoded CNTF protein in these mice. In contrast to the beneficial effects of CNTF in preventing motor neuron degeneration in other experimental paradigms, we report that overproduction of CNTF increased the rate of onset of motor disease symptoms in mnd mice and the presence of the transgene correlated with low adult body weight in mnd and wild-type genetic backgrounds.

摘要

睫状神经营养因子(CNTF)在体外和体内均可促进运动神经元的存活。此外,CNTF可阻止幼龄啮齿动物中受损或患病运动神经元的退化。运动神经元退化(mnd)突变小鼠表现出反映进行性运动功能衰弱的成年期症状,并提供了一个模型来检验CNTF可预防这些运动功能丧失的假说。我们培育出了携带基因组整合转基因的mnd小鼠,导致这些小鼠中编码的CNTF蛋白过表达。与CNTF在其他实验范式中预防运动神经元退化的有益作用相反,我们报告称,CNTF的过量产生增加了mnd小鼠运动疾病症状的发作速率,并且在mnd和野生型遗传背景中,转基因的存在与成年小鼠低体重相关。

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