Cortical transcriptome analysis after spinal cord injury reveals the regenerative mechanism of central nervous system in CRMP2 knock-in mice

Neural Regen Res, 2021 · DOI: 10.4103/1673-5374.301035 · Published: December 12, 2020

Spinal Cord Injury Neurology Bioinformatics

Simple Explanation

This study investigates the effects of inhibiting CRMP2 phosphorylation on spinal cord injury (SCI) pathophysiology in mice. CRMP2 is a protein involved in axon elongation and recovery after SCI. The researchers used CRMP2 knock-in (CRMP2KI) mice, which have a mutation that inhibits CRMP2 phosphorylation. They analyzed the structural changes and gene expression in the sensorimotor cortex of these mice after SCI. The findings suggest that inhibiting CRMP2 phosphorylation improves SCI pathophysiology by affecting microtubule stabilization, energy metabolism, glial cell responses, and synaptic function in the central nervous system.

Study Duration

4 weeks

Participants

Female wild-type (WT) and CRMP2KI (Crmp2KI/KI) mice

Evidence Level

Not specified

Key Findings

1
CRMP2KI suppresses somatic atrophy in sensorimotor cortex after spinal cord injury
2
CRMP2KI suppresses postsynaptic spine reduction in sensorimotor cortex after spinal cord injury
3
Four hemoglobin genes were remarkably upregulated after spinal cord injury in WT mice

Research Summary

This study aimed to reveal the intracellular mechanism in axotomized neurons in the CRMP2 knock-in (CRMP2KI) mouse model by performing transcriptome analysis in mouse sensorimotor cortex using micro-dissection punching system. Our results showed that CRMP2KI mice displayed improved SCI pathophysiology not only via microtubule stabilization in neurons, but also possibly via the whole metabolic system in the central nervous system, response changes in glial cells, and synapses. Taken together, we reveal new insights on SCI pathophysiology and the regenerative mechanism of central nervous system by the inhibition of CRMP2 phosphorylation at Ser522.

Practical Implications

Potential therapeutic target

CRMP2 phosphorylation inhibition could be a therapeutic target for SCI.

Understanding SCI pathophysiology

Study provides insights into the molecular mechanisms of SCI.

Improved recovery strategies

Findings may contribute to the development of improved recovery strategies for SCI.

Study Limitations

1
Locations that each protein works and protein interaction after SCI are not directly revealed.
2
Cell-to-cell interaction in cortex is also unclear.
3
In order to clarify the concrete mechanism on CNS regeneration, the complicated SCI pathophysiology and pathophysiological phenomena in CRMP2KI need to be further investigated.

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