Minor Kenneth, Tang Xiufeng, Kahrilas Genevieve, Archibald Simon J, Davies Jeannette E, Davies Stephen J
Department of Neurosurgery, Anschutz Medical Campus, University of Colorado at Denver, Neurosurgery Research Laboratory, Aurora, CO 80045, USA.
Neurobiol Dis. 2008 Oct;32(1):88-95. doi: 10.1016/j.nbd.2008.06.009. Epub 2008 Jun 26.
Inhibitory chondroitin sulfate proteoglycans (CSPGs) and myelin-associated molecules are major impediments to axon regeneration within the adult central nervous system (CNS). Decorin infusion can however suppress the levels of multiple inhibitory CSPGs and promote axon growth across spinal cord injuries [Davies, J.E., Tang, X., Denning, J.W., Archibald, S.J., and Davies, S.J., 2004. Decorin suppresses neurocan, brevican, phosphacan and NG2 expression and promotes axon growth across adult rat spinal cord injuries. Eur. J. Neurosci. 19, 1226-1242]. A question remained as to whether decorin can also increase axon growth on inhibitory CSPGs and myelin via a direct effect on neurons. We have therefore conducted an in vitro analysis of neurite extension by decorin-treated adult dorsal root ganglion (DRG) neurons cultured on substrates of inhibitory CSPGs or myelin membranes mixed with laminin. Decorin treatment promoted 14.5 and 5-fold increases in average neurite length/neuron over untreated controls on CSPGs or myelin membranes respectively. In addition to suppressing inhibitory scar formation, our present data shows that decorin can directly boost the ability of neurons to extend axons within CSPG or myelin rich environments.
抑制性硫酸软骨素蛋白聚糖（CSPGs）和髓磷脂相关分子是成年中枢神经系统（CNS）中轴突再生的主要障碍。然而，注入核心蛋白聚糖可以抑制多种抑制性CSPGs的水平，并促进轴突跨越脊髓损伤生长[戴维斯，J.E.，唐，X.，丹宁，J.W.，阿奇博尔德，S.J.，和戴维斯，S.J.，2004年。核心蛋白聚糖抑制神经聚糖、短蛋白聚糖、磷蛋白聚糖和NG2的表达，并促进轴突跨越成年大鼠脊髓损伤生长。欧洲神经科学杂志。19，1226 - 1242]。一个问题仍然存在，即核心蛋白聚糖是否也能通过对神经元的直接作用增加轴突在抑制性CSPGs和髓磷脂上的生长。因此，我们对在与层粘连蛋白混合的抑制性CSPGs或髓磷脂膜底物上培养的经核心蛋白聚糖处理的成年背根神经节（DRG）神经元的神经突延伸进行了体外分析。与未处理的对照组相比，核心蛋白聚糖处理分别使CSPGs或髓磷脂膜上每个神经元的平均神经突长度增加了14.5倍和5倍。除了抑制抑制性瘢痕形成外，我们目前的数据表明，核心蛋白聚糖可以直接增强神经元在富含CSPG或髓磷脂的环境中延伸轴突的能力。
