N-Acetylglucosamine 6-O-Sulfotransferase-1 is crucialenzyme for 5D4-reactive keratin sulfate biosynthesis which elicits expression after spinal cord injury.

：5D4-反应性KSPG在野生型小鼠CNS中随着年龄的增长而减少，并且在GlcNAc 6ST-1-/-小鼠中失去表达。另一方面，在野生型和GlcNAc 6ST- 1-/-小鼠CNS中，BCD 4反应性KSPG随着年龄的增长而增加。与野生型小鼠相比，在GlcNAc 6ST-1-/-小鼠的CNS中，KS酶b3 GlcNAcT-7不仅显著下调GlcNAc 6ST-1。对于GlcNAc 6ST-1 siRNA转染的BV 2的细胞裂解物，5D4反应性KSPG降低，尽管BCD 4反应性KSPG没有降低。与体内研究相同，不仅GlcNAc 6ST-1，b3 GlcNAcT-7也显著下调。显著下调的酶仅为b3 GlcNAcT-7。如果除BCD 4反应性KS外的5D 4反应性KS的消融是可能的，则可以获得更好的功能恢复。结果表明，GlcNAc 6ST-1是5D4反应性KSPGs生物合成的重要酶，b3 GlcNAcT-7是5D4和BCD 4反应性KSPGs生物合成的重要酶。使用转染的小胶质细胞系的体外研究支持该数据。有趣的是，GlcNAc 6ST-1可能通过降低自身表达来调节b3 GclNAcT-7。GlcNAc 6ST-1特异性下调治疗可能是CNS损伤的关键。

：5D4-reactive KSPGs were decrease as aging in wild type mice CNS, and were loss of expression in GlcNAc6ST-1-/- mice. On the other hand, BCD4-reactive KSPGs were increased as aging in wild type and GlcNAc6ST- 1-/- mice CNS. The KS enzyme b3GlcNAcT-7 was also significantly down-regulated not only GlcNAc6ST-1 in CNS of GlcNAc6ST-1-/- mice compared to that of wild type mice. 5D4-reactive KSPGs were decreased for cell lysates of GlcNAc6ST-1 siRNA transfected BV2, although BCD4-reactive KSPGs were not decreased. The enzyme b3GlcNAcT-7 was significantly downregulated not only GlcNAc6ST-1 same as in vivo study. The enzyme significantly down-regulated was only b3GlcNAcT-7. If the ablation of 5D4-reactive KS except for BCD4-reactive KS is possible, better functional recovery may be obtained. Ourdata suggested that GlcNAc6ST-1 was important enzyme for 5D4-reactive KSPGs biosynthesis, b3GlcNAcT-7 for both 5D4 and BCD4-reactive KSPGs biosynthesis. The data was supported with in vitro study used transfected microglia cell line. Interestingly, GlcNAc6ST-1 may regulate b3GclNAcT-7 by decrease of own expression. GlcNAc6ST-1 specific down-regulation treatment may be the key in CNS injury.