Keratan Sulfate Restricts Neural Plasticity after Spinal Cord Injury

The Journal of Neuroscience, 2011 · DOI: 10.1523/JNEUROSCI.5120-10.2011 · Published: November 23, 2011

Simple Explanation

This study investigates the role of keratan sulfate (KS) in neural plasticity following spinal cord injury (SCI). The researchers used an enzyme, keratanase II (K-II), to degrade KS in rats with SCI and observed the effects on motor and sensory function recovery. The study found that degrading KS with K-II promoted recovery of motor and sensory functions after SCI. This suggests that KS, similar to chondroitin sulfate (CS), inhibits the structural rearrangement of the neuronal network after injury. Further experiments indicated that the inhibitory activity of proteoglycans requires all three components: the core protein, CS chains, and KS chains. This means that both KS and CS independently contribute to the proteoglycan-mediated inhibition of axonal regeneration and sprouting.

Study Duration

10 weeks

Participants

Adult female Sprague Dawley rats weighing 200–230 g

Evidence Level

Not specified

Key Findings

1
K-II, an enzyme that specifically degrades KS, promoted motor and sensory function recovery in rats after SCI.
2
The effects of K-II were comparable to those of chondroitinase ABC (C-ABC), an enzyme that degrades CS, suggesting that KS has an impact comparable to CS on post-injury plasticity.
3
The study determined that KS and CS independently contribute to the proteoglycan-mediated inhibition of axonal regeneration and sprouting.

Research Summary

This study investigates the role of keratan sulfate (KS) in plasticity after spinal cord injury (SCI) by using keratanase II (K-II), an enzyme that specifically degrades KS in vivo. The main finding is that KS and CS have a comparable impact on post-injury plasticity, and both are independent requirements for the proteoglycan-mediated inhibition of axonal regeneration/sprouting. The study also determined the structural basis of proteoglycan-mediated inhibition of neural plasticity, suggesting that all three components of the proteoglycan moiety (core protein, CS chains, and KS chains) are required for the inhibitory activity of proteoglycans.

Practical Implications

Therapeutic Target for SCI

KS, like CS, can be targeted to promote neural plasticity and functional recovery after SCI.

Combination Therapies

Combining K-II and C-ABC may not lead to additive or synergistic effects, suggesting independent mechanisms of action.

Understanding Proteoglycan Structure

The core protein and both KS and CS chains are necessary for the inhibitory activity of proteoglycans, influencing future research directions.

Study Limitations

1
The exact mechanisms by which KS and CS independently inhibit neurite outgrowth remain unclear.
2
The study acknowledges that functional recovery induced by K-II or C-ABC was not complete, suggesting the need for additional therapeutic strategies such as rehabilitation.
3
The limited ability of the 5D4 antibody to detect KS might have affected the results.

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