Chondroitin sulphate N-acetylgalactosaminyl-transferase-1 inhibits recovery from neural injury View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-11-12

AUTHORS

Kosei Takeuchi, Nozomu Yoshioka, Susumu Higa Onaga, Yumi Watanabe, Shinji Miyata, Yoshino Wada, Chika Kudo, Masayasu Okada, Kentaro Ohko, Kanako Oda, Toshiya Sato, Minesuke Yokoyama, Natsuki Matsushita, Masaya Nakamura, Hideyuki Okano, Kenji Sakimura, Hitoshi Kawano, Hiroshi Kitagawa, Michihiro Igarashi

ABSTRACT

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 more completely from spinal cord injury than wild-type mice and even chondroitinase ABC-treated mice. Notably, synthesis of heparan sulphate (HS), a glycosaminoglycan promoting axonal growth, is also upregulated in TI knockout mice because HS-synthesis enzymes are induced in the mutant neurons. Moreover, chondroitinase ABC treatment never induces HS upregulation. Taken together, our results indicate that regulation of a single gene, T1, mediates excellent recovery from spinal cord injury by optimizing counteracting effectors of axon regeneration--an extracellular inhibitor of CS and intrinsic promoters, namely, HS-synthesis enzymes. More... »

PAGES

2740

Journal

TITLE

Nature Communications

ISSUE

1

VOLUME

4

Author Affiliations

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncomms3740

DOI

http://dx.doi.org/10.1038/ncomms3740

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1008776503

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24220492


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349 Department of Neurosurgery, Brain Research Institute, Niigata University, 1-757 Asahi-machi, Niigata 951 8510, Japan
350 rdf:type schema:Organization
351 grid-institutes:grid.272456.0 schema:alternateName Laboratory of Neural Regeneration, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Tokyo 156 8506, Japan
352 schema:name Laboratory of Neural Regeneration, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Tokyo 156 8506, Japan
353 rdf:type schema:Organization
354 grid-institutes:grid.411100.5 schema:alternateName Department of Biochemistry, Kobe Pharmaceutical University, 4-19-1 Motoyamakita-machi, Kobe 658 8558, Japan
355 schema:name Department of Biochemistry, Kobe Pharmaceutical University, 4-19-1 Motoyamakita-machi, Kobe 658 8558, Japan
356 rdf:type schema:Organization
357 grid-institutes:grid.452478.8 schema:alternateName Translational Research Center (TRC), Ehime University Hospital, Shitsukawa, Ehime 791-0295, Japan
358 schema:name Translational Research Center (TRC), Ehime University Hospital, Shitsukawa, Ehime 791-0295, Japan
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360 grid-institutes:grid.54432.34 schema:alternateName Doctoral and restart postdoctoral fellowship program, Japan Society for the Promotion of Science (JSPS), Tokyo 102 8472, Japan
361 schema:name Center for Transdisciplinary Research, Brain Research Institute, Niigata University, 1-757 Asahi-machi, Niigata 951 8510, Japan
362 Department of Neurochemistry and Molecular Cell Biology, Brain Research Institute, Niigata University, 1-757 Asahi-machi, Niigata 951 8510, Japan
363 Doctoral and restart postdoctoral fellowship program, Japan Society for the Promotion of Science (JSPS), Tokyo 102 8472, Japan
364 Laboratory of Neural Regeneration, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Tokyo 156 8506, Japan
365 rdf:type schema:Organization
 




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