The role of glycosaminoglycan in neuronal injuries

非允许性信号，如硫酸软骨素蛋白聚糖（CSPGs）和信号蛋白，在神经元损伤后抑制神经元轴突再生和胶质瘢痕。在这项研究中，我们主要研究硫酸软骨素（CS）和硫酸角蛋白（KS）对轴突再生的抑制活性。我们发现n -乙酰氨基葡萄糖6- o -磺基转移酶(GlcNAc6ST) -1参与中枢神经系统KS的生物合成。在皮质刺伤后，野生型小鼠在损伤部位诱导CS和KS表达，而gicnac6st缺陷小鼠仅诱导CS表达，而无法检测到KS。gicnac6st缺失小鼠比野生型小鼠表现出更多的轴突再生。为了进一步研究KS在神经元损伤中的作用，我们对脊髓进行了挫伤。与野生型小鼠相比，gicnac6st缺陷小鼠表现出胶质瘢痕形成减少，轴突再生增强，从而更好地恢复运动功能。我们的数据表明，KS在损伤后神经元轴突再生的抑制中起着不可或缺的作用。

Non-permissive cues, such as chondroitin sulfate proteoglycans (CSPGs) and semaphorin, inhibit neuronal axon regeneration together with glial scar after neuronal injuries. In this study we focused on chondroitin sulfate (CS) and keratan sulfate (KS) with regards to their inhibitory activity against axonal regeneration. We found that N-acetylglucosamine6-O-sulfotransferase (GlcNAc6ST) -1in involved in KS biosynthesis in the central nervous system. Upon cortical stab wound, CS and KS expression was induced at the injury site in wild-type mice, while CS expression was only induced but KS was undetectable in GIcNAc6ST-deficient mice. GIcNAc6ST-deficient mice showed more axonal regeneration than wild-type mice did. To further investigate the role of KS in neuronal injuries, we made contusion injuries to the spinal cord. GIcNAc6ST-deficient mice exhibited reduced glial scar formation, enhanced axonal regeneration and consequently better recovery of motor function as compared with wild-type mice. Our data suggest that KS plays an indispensable role in inhibition of neuronal axon regeneration after injuries.