Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
17
pubmed:dateCreated
2010-4-29
pubmed:abstractText
Neurons in the adult CNS do not spontaneously regenerate after injuries. The glycosaminoglycan keratan sulfate is induced after spinal cord injury, but its biological significance is not well understood. Here we investigated the role of keratan sulfate in functional recovery after spinal cord injury, using mice deficient in N-acetylglucosamine 6-O-sulfotransferase-1 that lack 5D4-reactive keratan sulfate in the CNS. We made contusion injuries at the 10th thoracic level. Expressions of N-acetylglucosamine 6-O-sulfotransferase-1 and keratan sulfate were induced after injury in wild-type mice, but not in the deficient mice. The wild-type and deficient mice showed similar degrees of chondroitin sulfate induction and of CD11b-positive inflammatory cell recruitment. However, motor function recovery, as assessed by the footfall test, footprint test, and Basso mouse scale locomotor scoring, was significantly better in the deficient mice. Moreover, the deficient mice showed a restoration of neuromuscular system function below the lesion after electrical stimulation at the occipito-cervical area. In addition, axonal regrowth of both the corticospinal and raphespinal tracts was promoted in the deficient mice. In vitro assays using primary cerebellar granule neurons demonstrated that keratan sulfate proteoglycans were required for the proteoglycan-mediated inhibition of neurite outgrowth. These data collectively indicate that keratan sulfate expression is closely associated with functional disturbance after spinal cord injury. N-acetylglucosamine 6-O-sulfotransferase-1-deficient mice are a good model to investigate the roles of keratan sulfate in the CNS.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
28
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5937-47
pubmed:meshHeading
pubmed-meshheading:20427653-Animals, pubmed-meshheading:20427653-Antigens, CD11b, pubmed-meshheading:20427653-Axons, pubmed-meshheading:20427653-Brain, pubmed-meshheading:20427653-Cells, Cultured, pubmed-meshheading:20427653-Chondroitin Sulfates, pubmed-meshheading:20427653-Female, pubmed-meshheading:20427653-Keratan Sulfate, pubmed-meshheading:20427653-Mice, pubmed-meshheading:20427653-Mice, Inbred C57BL, pubmed-meshheading:20427653-Mice, Knockout, pubmed-meshheading:20427653-Motor Activity, pubmed-meshheading:20427653-Nerve Regeneration, pubmed-meshheading:20427653-Neural Pathways, pubmed-meshheading:20427653-Neurites, pubmed-meshheading:20427653-Neuromuscular Junction, pubmed-meshheading:20427653-Rats, pubmed-meshheading:20427653-Rats, Sprague-Dawley, pubmed-meshheading:20427653-Recovery of Function, pubmed-meshheading:20427653-Spinal Cord Injuries, pubmed-meshheading:20427653-Sulfotransferases
pubmed:year
2010
pubmed:articleTitle
N-acetylglucosamine 6-O-sulfotransferase-1-deficient mice show better functional recovery after spinal cord injury.
pubmed:affiliation
Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't