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Glycobiology Advance Access published online on April 19, 2006
Glycobiology, doi:10.1093/glycob/cwj115
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org
Received December 17, 2005
Revised March 28, 2006
Accepted April 10, 2006

Article

N-acetylglucosamine 6-O-sulfotransferase-1 is required for brain keratan sulfate biosynthesis and glial scar formation after brain injury

Haoqian Zhang 1, Takashi Muramatsu 2 *, Atsushi Murase 1, Shigeki Yuasa 3, Kenji Uchimura 4, and Kenji Kadomatsu 5 *

1 Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan
2 Department of Health Science, Faculty of Psychological and Physical Sciences, Aichi Gakuin University, Aichi 470-0195, Japan
3 Department of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187-8502, Japan
4 Department of Anatomy, Program in Immunology, University of California, San Francisco, California 94143, USA
5 Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan; Institute for Advanced Research, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan

* To whom correspondence should be addressed.
Takashi Muramatsu, E-mail: tmurama{at}dpc.aichi-gakuin.ac.jp
Kenji Kadomatsu, E-mail: kkadoma{at}med.nagoya-u.ac.jp


  Abstract

Keratan sulfate is a glycosaminoglycan composed of repeating disaccharide units with sulfate residues at the C6 positions of galactose and N-acetylglucosamine. The N-acetylglucosamine 6-O-sulfotransferase(s) involved in the synthesis of keratan sulfate in the central nervous system has long been unidentified. Here we report that a deficiency of N-acetylglucosamine 6-O-sulfotransferase-1 leads to loss of 5D4-reactive brain keratan sulfate and reduction of glial scar formation after cortical stab injury in mice. During the development of mice deficient in N-acetylglucosamine 6-O-sulfotransferase-1, keratan sulfate expression in the brain was barely detectable with the keratan sulfate-specific antibody 5D4. The reactivity of 5D4 antibody with protein tyrosine phosphatase {zeta}, a keratan sulfate proteoglycan, was abolished in the deficient mice. In adults, brain injury induced 5D4-reactive keratan sulfate synthesis in the wounded area in wild-type but not in the deficient mice. Glial scar is formed via accumulation of reactive astrocytes and is a major obstacle to axonal regeneration by injured neurons. Reactive astrocytes appeared to similar extents in the two genotypes, but they accumulated in the wounded area to a lesser extent in the deficient mice. Consequently, the deficient mice exhibited a marked reduction of scarring and enhanced neuronal regeneration after brain injury. These findings highlight the indispensable role of N-acetylglucosamine 6-O-sulfotransferase-1 in brain keratan sulfate biosynthesis and glial scar formation after brain injury.

Keywords: N-acetylglucosamine 6-O-sulfotransferase/keratan sulfate/reactive astrocytes/glial scar/axon regeneration.
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