MicroRNA-219 Inhibits Proliferation and Induces Differentiation of Oligodendrocyte Precursor Cells after Contusion Spinal Cord Injury in Rats

Neural Plasticity, 2019 · DOI: https://doi.org/10.1155/2019/9610687 · Published: February 18, 2019

Simple Explanation

Spinal cord injuries often lead to lasting sensorimotor dysfunction, impacting the quality of life. A key aspect of this injury involves the death of oligodendrocytes, cells responsible for myelinating axons, leading to demyelination. Promoting remyelination is a potential treatment strategy. MicroRNAs, like miR-219, are small RNA molecules that regulate gene expression. MiR-219 is known to influence the development of the central nervous system by affecting oligodendrocyte precursor cells (OPCs). This study investigates whether miR-219 can modulate OPC proliferation and differentiation after spinal cord injury. The study found that after spinal cord injury, miR-219 levels decreased, while the number of OPCs and astrocytes increased. Overexpressing miR-219 increased the number of oligodendrocytes and suppressed the generation of OPCs and astrocytes, suggesting miR-219 plays a role in mediating OPC behavior after SCI.

Study Duration

14 days

Participants

160 male Sprague-Dawley rats

Evidence Level

Level 2: Experimental study in rats

Key Findings

1
SCI downregulates miR-219 expression at the lesion center of the injured spinal cord tissues in the acute and sub-acute SCI phases, with the lowest level of miR-219 expression occurring on day 7 after injury.
2
Elevation of miR-219 in vivo resulted in a significant increase in the number of OLs and a decrease in the number of proliferating OPCs and As.
3
MiR-219 may increase ipsilateral forelimb usage and forepaw range of motion in contusion SCI rats, promoting the recovery of forelimb motor function.

Research Summary

This study investigates the role of microRNA-219 (miR-219) in modulating oligodendrocyte precursor cell (OPC) proliferation and differentiation following contusion spinal cord injury (SCI) in rats. The findings indicate that SCI leads to decreased miR-219 expression, increased OPC and astrocyte numbers, and decreased oligodendrocyte numbers. Overexpression of miR-219 promotes oligodendrocyte generation and suppresses OPC and astrocyte formation, suggesting a crucial role for miR-219 in OPC fate determination after SCI. The study also suggests that monocarboxylate transporter 1 (MCT-1) may mediate the effects of miR-219 on OPC differentiation, potentially serving as a therapeutic target for promoting functional recovery after SCI.

Practical Implications

Therapeutic Target for SCI

MiR-219 may represent a novel therapeutic target for promoting functional recovery after contusion spinal cord injury.

Promoting Remyelination

Upregulating miR-219 expression may promote remyelination after SCI.

Understanding OPC Differentiation

Further research into the regulatory roles of miR-219 and MCT-1 in OPC proliferation and differentiation following SCI is warranted.

Study Limitations

1
Schwann cells might mediate remyelination of injured spinal axons, therefore, average optical density of the MBP stained area represented the number of OLs after SCI showed certain limitation.
2
LFB staining has certain specificity and is a good staining method for identifying myelin, but it cannot distinguish old myelin from new myelin post-SCI.
3
It remains unclear whether the miR-219-associated increase in MCT-1 is related to its role in OPC proliferation and differentiation.

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