The role of glycosaminoglycan in neuronal injuries

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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.