Di Giorgio Francesco Paolo, Carrasco Monica A, Siao Michelle C, Maniatis Tom, Eggan Kevin
The Stowers Medical Institute, the Harvard Stem Cell Institute. Harvard University, 7 Divinity Ave., Cambridge, Massachusetts 02138, USA.
Nat Neurosci. 2007 May;10(5):608-14. doi: 10.1038/nn1885. Epub 2007 Apr 15.
Here we report an in vitro model system for studying the molecular and cellular mechanisms that underlie the neurodegenerative disease amyotrophic lateral sclerosis (ALS). Embryonic stem cells (ESCs) derived from mice carrying normal or mutant transgenic alleles of the human SOD1 gene were used to generate motor neurons by in vitro differentiation. These motor neurons could be maintained in long-term coculture either with additional cells that arose during differentiation or with primary glial cells. Motor neurons carrying either the nonpathological human SOD1 transgene or the mutant SOD1(G93A) allele showed neurodegenerative properties when cocultured with SOD1(G93A) glial cells. Thus, our studies demonstrate that glial cells carrying a human SOD1(G93A) mutation have a direct, non-cell autonomous effect on motor neuron survival. More generally, our results show that ESC-based models of disease provide a powerful tool for studying the mechanisms of neural degeneration. These phenotypes displayed in culture could provide cell-based assays for the identification of new ALS drugs.
在此,我们报道了一种体外模型系统,用于研究神经退行性疾病肌萎缩侧索硬化症(ALS)背后的分子和细胞机制。利用携带人SOD1基因正常或突变转基因等位基因的小鼠胚胎干细胞(ESC),通过体外分化生成运动神经元。这些运动神经元可以与分化过程中产生的其他细胞或原代神经胶质细胞进行长期共培养。携带非病理性人SOD1转基因或突变SOD1(G93A)等位基因的运动神经元在与SOD1(G93A)神经胶质细胞共培养时表现出神经退行性特性。因此,我们的研究表明,携带人SOD1(G93A)突变的神经胶质细胞对运动神经元存活具有直接的、非细胞自主性的影响。更普遍地说,我们的数据表明基于ESC的疾病模型为研究神经变性机制提供了一个强大的工具。在培养中显示的这些表型可为鉴定新的ALS药物提供基于细胞的检测方法。