Regulation of the chondroitin sulfate and recovery systems from the spinal cord injury.

抑制轴突生长的细胞外因素和促进轴突生长的内在因素影响神经再生。针对任何单一基因的疗法尚未同时优化这两种类型的因子。硫酸软骨素（CS），一种糖胺聚糖，是最丰富的轴突生长的细胞外抑制剂。在此，我们发现，携带CS N-乙酰氨基半乳糖转移酶-1（T1）（CS生物合成的关键酶）基因敲除的小鼠，比野生型小鼠，甚至比软骨素酶ABC处理的小鼠，从脊髓损伤中恢复得更完全。总之，我们的研究结果表明，调节单个基因T1，通过优化轴突再生的抵消效应，介导了脊髓损伤的良好恢复

Extracellular factors that inhibit axon growth and intrinsic factors that promote it affect neural regeneration. Therapies targeting any single gene have not yet simultaneously optimized both types of factors. Chondroitin sulphate (CS), a glycosaminoglycan, is the most abundant extracellular inhibitor of axon growth. Here we show that mice carrying a gene knockout for CS N-acetylgalactosaminyltransferase-1 (T1), a key enzyme in CS biosynthesis, recover morecompletely from spinal cord injury than wild-type mice and even chondroitinase ABC-treated mice.Taken together, our results indicate that regulation of a single gene, T1, mediates excellent recovery from spinal cord injury by optimizing counteracting effectorsof axon regeneration