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MicroRNA339 Targeting PDXK Improves Motor Dysfunction and Promotes Neurite Growth in the Remote Cortex Subjected to

Liu-Lin Xiong^1,2,3, Yan-Xia Qin⁴, Qiu-Xia Xiao²

¹Institute of Neurobiological Disease, Department of Anesthesiology, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, China.

Frontiers in Cell and Developmental Biology

|August 15, 2020

Summary

Researchers found that inhibiting miR-339 in the motor cortex promotes nerve regeneration and motor function recovery after spinal cord injury (SCI). This discovery offers a potential new therapeutic strategy for SCI patients.

Keywords:

PDXK RNA interference microRNA339 motor cortex plasticity spinal cord injury

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Area of Science:

Neuroscience
Molecular Biology
Regenerative Medicine

Background:

Spinal cord injury (SCI) leads to severe disability, with limited understanding of molecular mechanisms for functional recovery.
Cortical reorganization plays a role in spontaneous function recovery after SCI, but remote regulatory pathways remain unclear.

Purpose of the Study:

To investigate the molecular mechanisms of neurological improvement and motor function recovery after spinal cord transection (SCT) via remote cerebral cortex regulation.
To identify key molecular targets and pathways involved in functional recovery post-SCI.

Main Methods:

Proteomics analysis, RNA interference/overexpression, and CRISPR/Cas9 were employed both in vivo and in vitro.
Investigated the role of pyridoxal kinase (PDXK) and its regulation by microRNA-339 (miR-339).
Assessed functional recovery using the Basso, Beattie, and Bresnehan (BBB) score in rat models.

Main Results:

Overexpression of PDXK in the motor cortex enhanced neuronal growth, survival, and hindlimb locomotor function.
PDXK was identified as a target of miR-339; miR-339 knockout (KO) increased neurite outgrowth and decreased apoptosis in cortical neurons.
miR-339 KO rats showed significant functional recovery, evidenced by improved BBB scores, linked to PDXK and GAP43 regulation.

Conclusions:

The miR-339 targeting of PDXK in the motor cortex facilitates neurological recovery after SCT.
The underlying mechanism involves regulating GAP43 in the remote cortex, offering insights into remote cortex control post-SCI.
This study presents a potential new therapeutic strategy for SCI recovery.