Simonin Yannick, Charron Yves, Sonderegger Peter, Vassalli Jean-Dominique, Kato Ann C
Department of Basic Neurosciences, Faculty of Medicine, University of Geneva, CH-1211 Geneva, Switzerland.
J Neurosci. 2006 Oct 11;26(41):10614-9. doi: 10.1523/JNEUROSCI.3582-06.2006.
Various studies suggest that proteolytic activity may be involved in a number of neurodegenerative disorders, including stroke and seizure. In this report, we examined the role of tryptic serine proteases, plasminogen activators (PAs), in the evolution of a neurodegenerative disease. Transgenic mice overexpressing an axonally secreted inhibitor of serine proteases (neuroserpin) were crossed with mice characterized by a "dying-back" motor neuron disease [progressive motor neuronopathy (pmn/pmn)]. Compared with pmn/pmn mice that showed an increase in PA activity, double mutant mice had decreased PA activity in sciatic nerves and spinal cord; their lifespan was increased by 50%, their motor behavior was stabilized, and histological analysis revealed increased numbers of myelinated axons and rescue of motoneuron number and size. This is the first report showing that a class of serine proteases (PAs) may be involved in the pathogenesis of a motor neuron disease and more specifically in axonal degeneration. Inhibiting serine proteases could offer a new strategy for delaying these disorders.
多项研究表明,蛋白水解活性可能与包括中风和癫痫在内的多种神经退行性疾病有关。在本报告中,我们研究了胰蛋白酶丝氨酸蛋白酶即纤溶酶原激活剂(PAs)在一种神经退行性疾病发展过程中的作用。将过度表达轴突分泌型丝氨酸蛋白酶抑制剂(神经丝氨酸蛋白酶抑制剂)的转基因小鼠与以“逆行性”运动神经元疾病[进行性运动神经元病(pmn/pmn)]为特征的小鼠进行杂交。与显示PA活性增加的pmn/pmn小鼠相比,双突变小鼠坐骨神经和脊髓中的PA活性降低;它们的寿命延长了50%,运动行为得到稳定,组织学分析显示有髓轴突数量增加,运动神经元的数量和大小得到挽救。这是第一份表明一类丝氨酸蛋白酶(PAs)可能参与运动神经元疾病发病机制,更具体地说是参与轴突变性的报告。抑制丝氨酸蛋白酶可能为延缓这些疾病提供一种新策略。