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Author Notes:

Robert McKeon, Department of Cell Biology, Emory University School of Medicine, 1648 Pierce Drive, Atlanta, GA 30322-3030. E-mail: mckeon@cellbio.emory.edu

We thank Dr. Yu Yamaguchi (The Burnham Institute) and Dr. Richard LeBaron (University of Texas-San Antonio) for antibodies to specific CS-PGs; and Anthony Frankfurter (University of Virginia) for the antibody to neuron-specific β-tubulin.

Antibodies to neurocan (1F6) and phosphacan (3F8) were obtained from the Developmental Studies Hybridoma Bank maintained by the University of Iowa, Department of Biological Sciences, Iowa City, IA 52242.

We thank Catherine Riley and Anne Mongiu for excellent technical assistance.

Subjects:

Research Funding:

This work was supported by Spinal Cord Research Foundation of the Paralyzed Veterans of America; National Institutes of Health Grant NS-35986; and the Office of the Dean of Research, Emory University.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Neurosciences
  • Neurosciences & Neurology
  • chondroitin sulfate proteoglycans
  • reactive astrocytes
  • glial scars
  • axonal regeneration
  • CNS injury
  • gene expression
  • PROTEIN-TYROSINE-PHOSPHATASE
  • CENTRAL-NERVOUS-SYSTEM
  • CELL-ADHESION MOLECULES
  • GROWTH-FACTOR-BETA
  • NEURITE OUTGROWTH INHIBITOR
  • 6B4 PROTEOGLYCAN/PHOSPHACAN
  • BRAIN INJURY
  • EXTRACELLULAR VARIANT
  • NG2 PROTEOGLYCAN
  • GENE-EXPRESSION

The chondroitin sulfate proteoglycans neurocan and phosphacan are expressed by reactive astrocytes in the chronic CNS glial scar

Tools:

Journal Title:

Journal of Neuroscience Nursing

Volume:

Volume 19, Number 24

Publisher:

, Pages 10778-10788

Type of Work:

Article | Final Publisher PDF

Abstract:

Chondroitin sulfate proteoglycans (CS-PGs) expressed by reactive astrocytes may contribute to the axon growth-inhibitory environment of the injured CNS. The specific potentially inhibitory CS-PGs present in areas of reactive gliosis, however, have yet to be thoroughly examined. In this study, we used immunohistochemistry, combined immunohistochemistry-in situ hybridization, immunoblot analysis, and reverse transcription-PCR to examine the expression of specific CS-PGs by reactive astrocytes in an in vivo model of reactive gliosis: that is, the glial scar, after cortical injury. Neurocan and phosphacan can be localized to reactive astrocytes 30 d after CNS injury, whereas brevican and versican are not expressed in the chronic glial scar. Neurocan is also expressed by astrocytes in primary cell culture. Relative to the amount present in cultured astrocytes or uninjured cortex, neurocan expression increases significantly in the glial scar resulting from cortical injury, including the reexpression of the neonatal isoform of neurocan. In contrast, phosphacan protein levels are decreased in the glial scar compared with the uninjured brain. Because these CS-PGs are capable of inhibiting neurite outgrowth in vitro, our data suggest that phosphacan and neurocan in areas of reactive gliosis may contribute to axonal regenerative failure after CNS injury.

Copyright information:

Copyright © 1999 Society for Neuroscience

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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