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  4. Scar-mediated inhibition and CSPG receptors in the CNS

Scar-mediated inhibition and CSPG receptors in the CNS

Exp Neurol, 2012 · DOI: 10.1016/j.expneurol.2012.07.009 · Published: October 1, 2012

Spinal Cord InjuryRegenerative MedicineNeurology

Simple Explanation

After a CNS injury, severed axons in adult mammals do not regenerate appreciably due to a reduction in neuron-intrinsic growth capacity and inhibitory extracellular environment. Chondroitin sulfate proteoglycans (CSPGs), generated by scar tissues, contribute to this limiting environment. The main in vivo approach to overcoming inhibition by CSPGs is enzymatic digestion with chondroitinase ABC (ChABC). Recent studies indicate that protein tyrosine phosphatase σ (PTPσ) and LAR, are functional receptors that bind CSPGs with high affinity and mediate CSPG inhibitory effects. CSPGs also may act by binding to two receptors for myelin-associated growth inhibitors, Nogo receptors 1 and 3 (NgR1 and NgR3), suggesting that CSPGs have multiple mechanisms by which they inhibit axon growth.

Study Duration
Not specified
Participants
Not specified
Evidence Level
Review

Key Findings

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    Two members of the LAR phosphatase subfamily, PTPσ and LAR, are functional receptors that bind CSPGs with high affinity and mediate CSPG inhibitory effects.
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    CSPGs may also inhibit axon growth by binding to Nogo receptors 1 and 3 (NgR1 and NgR3), which are receptors for myelin-associated growth inhibitors.
  • 3
    The inhibitory actions of CSPGs are dependent on the sulfation pattern of GAG chains, as preventing GAG sulfation eliminates much of the inhibitory activity on axon growth in vitro.

Research Summary

This review focuses on CSPG-mediated inhibition and CSPG receptors identified recently, as severed axons in adult mammals do not regenerate appreciably after central nervous system (CNS) injury due to developmentally determined reductions in neuron-intrinsic growth capacity and extracellular environment for axon elongation. CSPGs were found to bind and block the normal growth-promoting properties of laminin. Recent evidence suggests that CSPGs also may bind to members of at least two distinct classes of growth-inhibitory receptors expressed on the surfaces of axons and thereby activate specific growth-inhibitory pathways. Identification of CSPG receptors is an important advance for better understanding the scar-mediated suppression, but many questions remain unanswered regarding the CSPG receptor-mediated suppression on neuronal growth.

Practical Implications

Therapeutic Target Identification

Identifying CSPG receptors like PTPσ and LAR offers novel therapeutic targets for promoting axon sprouting and regeneration after CNS injuries.

Combinatorial Therapies

Combining treatments that target both extracellular inhibitory factors (CSPGs) and neuron-intrinsic factors (PTEN, mTOR) may lead to more robust axon regeneration and neuronal plasticity.

Peptide-Based Therapies

Systemic application of LAR antagonistic peptides may provide a basis for achieving effective axonal regeneration and locomotor recovery in adult mammals with CNS injury.

Study Limitations

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