The neuronal differentiation microenvironment is essential for spinal cord injury repair

Organogenesis, 2017 · DOI: 10.1080/15476278.2017.1329789 · Published: May 8, 2017

Simple Explanation

Spinal cord injuries often result in significant disabilities due to the loss of motor function and sensation below the injury site. Neural stem cells (NSCs) hold promise for repairing these injuries. However, NSCs often differentiate into astrocytes instead of neurons due to the unfavorable environment after SCI. The presence of myelin-associated inhibitors (MAIs) contributes to this issue. By using a collagen scaffold with an anti-EGFR antibody, researchers aimed to counteract the effects of MAIs and create an environment that encourages NSCs to develop into neurons, ultimately promoting functional recovery after SCI.

Study Duration

Not specified

Participants

Animal models (rats and canines) of complete spinal cord transection

Evidence Level

Not specified

Key Findings

1
Myelin-associated inhibitors (MAIs) inhibit neuronal differentiation of NSCs.
2
Collagen scaffolds modified with anti-EGFR antibody prevent the inhibition of NSC neuronal differentiation by myelin.
3
Scaffold-linked antibodies induced production of nascent neurons from endogenous and transplanted NSCs, rebuilding neuronal relays and promoting functional recovery in SCI animals.

Research Summary

Spinal cord injury (SCI) often results in substantial disability. Neural stem cells (NSCs) are a promising strategy for SCI repair, but NSCs rarely differentiate into neurons because of the adverse microenvironment present after SCI. Myelin-associated inhibitors (MAIs) inhibit neuronal differentiation of NSCs. A collagen scaffold modified with anti-EGFR antibody prevented the inhibition of NSC neuronal differentiation by myelin. The scaffold-linked antibodies induced production of nascent neurons from endogenous and transplanted NSCs, which rebuilt the neuronal relay by forming connections with each other or host neurons to transmit electrophysiological signals and promote functional recovery.

Practical Implications

Therapeutic Strategy for SCI

Rebuilding the neuronal differentiation microenvironment with biomaterials could be a useful strategy for SCI repair.

Targeting EGFR Signaling

Attenuating EGFR signaling using anti-EGFR antibodies can promote neuronal differentiation of NSCs in the context of SCI.

Biomaterial Design

Collagen scaffolds can be modified with functional biomolecules, such as anti-EGFR antibodies, to create a regenerative microenvironment for SCI repair.

Study Limitations

1
The corticospinal tract (CST) fibers did not regenerate across the lesion in our SCI model.
2
Inadequate regenerative ability of central nervous system axons after SCI.
3
The inhibitive pathophysiological microenvironment present after SCI.

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