The chondroitin sulfate proteoglycans neurocan, brevican, phosphacan, and versican are differentially regulated following spinal cord injury

@article{Jones2003TheCS,
  title={The chondroitin sulfate proteoglycans neurocan, brevican, phosphacan, and versican are differentially regulated following spinal cord injury},
  author={Leonard L. Jones and Richard U. Margolis and Mark H. Tuszynski},
  journal={Experimental Neurology},
  year={2003},
  volume={182},
  pages={399-411}
}
Axonal Regeneration through Regions of Chondroitin Sulfate Proteoglycan Deposition after Spinal Cord Injury: A Balance of Permissiveness and Inhibition
TLDR
Examination of growth responses of axons to this inhibitory environment in the presence of a cellular fibroblast bridge in a spinal cord lesion site and after a growth factor stimulus shows that regeneration is successful when local permissive signals balance and exceed inhibitory signals.
Decorin suppresses neurocan, brevican, phosphacan and NG2 expression and promotes axon growth across adult rat spinal cord injuries
TLDR
The ability of decorin to promote axon growth across acute spinal cord injuries via a coordinated suppression of inflammation, CSPG expression and astroglial scar formation make decorin treatment a promising component of future spinal cord regeneration strategies.
The roles of neuronal and glial precursors in overcoming chondroitin sulfate proteoglycan inhibition
Chondroitinase ABC Promotes Sprouting of Intact and Injured Spinal Systems after Spinal Cord Injury
TLDR
Robust sprouting is found of both injured and intact descending projections as well as uninjured primary afferents after a cervical dorsal column injury and ChABC treatment and CSPG degradation; compensatory sprouting of descending systems could be a key mechanism underlying functional recovery.
Astrocytic and Vascular Remodeling in the Injured Adult Rat Spinal Cord after Chondroitinase ABC Treatment
TLDR
Interestingly, ChABC treatment favored an orientation of astrocytic processes directed toward the injury, in close association with axons at the lesion entry zone, suggesting a corr...
Role of chondroitin sulfate proteoglycans (CSPGs) in synaptic plasticity and neurotransmission in mammalian spinal cord.
TLDR
It is suggested that antagonism of proteoglycans reverses or prevents the decline of axonal conduction, in addition to stimulating axonal growth.
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References

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Chondroitin Sulfate Proteoglycan Immunoreactivity Increases Following Spinal Cord Injury and Transplantation
TLDR
Interestingly, the robust, injury-induced CSPG-IR patterns were not altered by intraspinal grafts of fetal spinal cord, and correlations in the injured and transplanted spinal cord support CSPGs' putative growth inhibitory effect in the adult spinal cord.
Spinal Cord Injury Elicits Expression of Keratan Sulfate Proteoglycans by Macrophages, Reactive Microglia, and Oligodendrocyte Progenitors
TLDR
The robust and extensive production of 5D4-KSPG at sites of SCI precedes the expression of other putatively inhibitory proteoglycan molecules such as chondroitin sulfate proteoglycans, and is the first demonstration that KSPGs are expressed after SCI in a temporal and spatial relationship that could exert an early and important role in modulating axonal growth afterSCI.
The Chondroitin Sulfate Proteoglycans Neurocan and Phosphacan Are Expressed by Reactive Astrocytes in the Chronic CNS Glial Scar
TLDR
The data suggest that phosphacan and neurocan in areas of reactive gliosis may contribute to axonal regenerative failure after CNS injury, and are capable of inhibiting neurite outgrowth in vitro.
NG2 Is a Major Chondroitin Sulfate Proteoglycan Produced after Spinal Cord Injury and Is Expressed by Macrophages and Oligodendrocyte Progenitors
TLDR
Evaluation of total soluble CSPGs 2 weeks after dorsal column lesion in the rat demonstrated that NG2 is highly upregulated and is a major CSPG species, a major component of this putatively inhibitory class of ECM molecules expressed at sites of SCI and may restrict axonal regeneration.
The chondroitin sulphate proteoglycan brevican is upregulated by astrocytes after entorhinal cortex lesions in adult rats
TLDR
Data demonstrate that brevican is upregulated in areas of brain damage as well as in areas denervated by a lesion, and suggest a role of brevicans in reactive gliosis and are compatible with the hypothesis that breVican is involved in the synaptic reorganization of denervate brain areas.
Inhibitory Proteoglycan Immunoreactivity Is Higher at the Caudal Than the Rostral Schwann Cell Graft-Transected Spinal Cord Interface
TLDR
The pattern of expression of inhibitory chondroitin sulfate proteoglycans 3 weeks after transplantation into completely transected adult rat thoracic spinal cord is determined, and the CSPGs studied are increased at 3 weeks, especially at the caudal SC graft-cord interface, possibly contributing to an inhibitory molecular barrier that precludes regrowing descending axons from entering the caUDal host cord.
Chondroitinase ABC promotes functional recovery after spinal cord injury
TLDR
It is demonstrated that CSPGs are important inhibitory molecules in vivo and suggested that their manipulation will be useful for treatment of human spinal injuries.
The Brain Chondroitin Sulfate Proteoglycan Brevican Associates with Astrocytes Ensheathing Cerebellar Glomeruli and Inhibits Neurite Outgrowth from Granule Neurons
TLDR
It is suggested that brevican presented on the surface of neuroglial sheaths may be controlling the infiltration of axons and dendrites into maturing glomeruli in brain development.
Versican Is Upregulated in CNS Injury and Is a Product of Oligodendrocyte Lineage Cells
TLDR
Results suggest that OLC-derived versican contributes to the inhospitable environment of the injured CNS and provides evidence of a role for CS-PGs in the axon growth-inhibitory properties of oligodendrocytes.
Increased expression of the NG2 chondroitin-sulfate proteoglycan after brain injury
  • J. Levine
  • Biology
    The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 1994
TLDR
Observations demonstrate that the cells that express the NG2 proteoglycan are a reactive cell type that responds to brain injury and may contribute to the failure of damaged CNS axons to regenerate successfully.
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