Gene silencing NMII promotes axonal regeneration against contusive spinal cord injury in rats

Int J Clin Exp Pathol, 2017 · DOI: · Published: November 15, 2017

Spinal Cord Injury Biochemistry Regenerative Medicine & Stem Cells

Simple Explanation

Spinal cord injury (SCI) often results in limited axon growth, hindering recovery. Non-muscle myosin II (NMII) influences cell structure, and silencing it can boost axon growth in lab settings. This study aims to explore the link between phosphorylated NMII and axon regeneration after SCI in rats. It also investigates whether silencing NMII can enhance locomotor function in rats with SCI. The findings suggest that elevated phosphorylated NMII after SCI may impede neuron survival and axon regeneration. Silencing NMII promoted neuron viability, axon proliferation, synaptic connection, and locomotor functional recovery.

Study Duration

8 weeks

Participants

Forty female adult Wistar rats

Evidence Level

Not specified

Key Findings

1
Phosphorylated NMII level was up-regulated after SCI, suggesting it may inhibit neuronal survival and axonal regeneration.
2
Silencing NMII promoted the viability of neurons, proliferation of axons, and synaptic connection after SCI.
3
Silencing NMII significantly improved locomotor functional recovery in rats after SCI.

Research Summary

This study investigates the impact of gene silencing non-muscle myosin II (NMII) on axonal regeneration following spinal cord injury (SCI) in rats. The research demonstrates that phosphorylated NMII levels increase after SCI and may inhibit neuronal survival and axonal regeneration. Silencing NMII promotes neuron viability, axon proliferation, synaptic connection, and locomotor functional recovery after SCI, suggesting a potential therapeutic approach for SCI.

Practical Implications

Therapeutic Target

NMII is a potential therapeutic target for promoting axonal regeneration and functional recovery after SCI.

Treatment Strategy

Gene silencing of NMII could be a novel method for repairing SCI by directly regulating neuron viability and axon proliferation.

Further Research

Further investigation is needed to elucidate the specific signaling pathway mechanisms involved in the recovery process after NMII silencing.

Study Limitations

1
Specific signaling pathway mechanisms require further study.
2
The reason why neuron collapse followed phosphorylated NMII is still uncertain.
3
Glial scar formation cannot be inhibited by silencing NMII.

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