Corticospinal tract regeneration after spinal cord injury in receptor protein tyrosine phosphatase sigma deficient mice
Abstract
Receptor protein tyrosine phosphatase sigma (RPTPσ) plays a role in inhibiting axon growth during development. It has also been shown to slow axon regeneration after peripheral nerve injury and inhibit axon regeneration in the optic nerve. Here, we assessed the ability of the corticospinal tract (CST) axons to regenerate after spinal hemisection and contusion injury in RPTPσ deficient (RPTPσ−/−) mice. We show that damaged CST fibers in RPTPσ−/− mice regenerate and appear to extend for long distances after a dorsal hemisection or contusion injury of the thoracic spinal cord. In contrast, no long distance axon regeneration of CST fibers is seen after similar lesions in wild‐type mice. In vitro experiments indicate that cerebellar granule neurons from RPTPσ−/− mice have reduced sensitivity to the inhibitory effects of chondroitin sulfate proteoglycan (CSPG) substrate, but not myelin, which may contribute to the growth of CST axons across the CSPG‐rich glial scar. Our data suggest that RPTPσ may function to prevent axonal growth after injury in the adult mammalian spinal cord and could be a target for promoting long distance regeneration after spinal cord injury. © 2009 Wiley‐Liss, Inc.
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RPTPσ binds with high affinity to neurocan and aggrecan and strongly inhibits axon outgrowth and regeneration.
“RPTPσ can bind with high affinity to neurocan and aggrecan and strongly inhibits axon outgrowth and regeneration (Sapieha et al., 2005;Shen et al., 2009;Fry et al., 2010;Lang et al., 2015).”
From The hyaluronan and proteoglycan link proteins: Organizers of the brain extracellular matrix and key molecules for neuronal function and plasticity (2015) · cites this paper as Fry et al., 2010
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- Authors
- Fry, E. J., Chagnon, M. J., López‐Vales, R., Tremblay, M. L., & David, S.
- Affiliations
- Research Institute of the McGill University Health Centre (CA)
- Corresponding author
- Tremblay, Michel L.
- David, Samuel
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2009-09-24
- Volume
- 58
- Issue
- 4
- Pages
- 423-433
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- OpenAlex
- W2007067483
- Cited by
- 152
- References
- 38
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 1 · 2023: 3 · 2022: 6 · 2021: 4 · 2020: 11 · 2019: 5 · 2018: 11 · 2017: 7 · 2016: 7 · 2015: 14 · 2014: 25 · 2013: 16 · 2012: 13
- FWCI
- 4.99
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research (42482_1, MT-15122)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- corticospinal tract, axon regeneration, spinal cord injury, spinal hemisection, bruising, chondroitin sulfate proteoglycans, glial scar, cerebellar granule cells, myelin, axon growth inhibition
- MeSH terms
- Animals, Axons, Cells, Cultured, Cerebellum, Female, Mice, Inbred BALB C, Myelin Sheath, Nerve Regeneration, Neurons, Chondroitin Sulfate Proteoglycans, Pyramidal Tracts, Spinal Cord Injuries, Mice, Knockout, Mice, Receptor-Like Protein Tyrosine Phosphatases, Class 2
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