Inhibition of LncRNA Vof-16 expression promotes nerve regeneration and functional recovery after spinal cord injury

Neural Regeneration Research, 2022 · DOI: https://doi.org/10.4103/1673-5374.314322 · Published: January 1, 2022

Simple Explanation

This study investigates the role of a specific long non-coding RNA, lncRNA Vof-16, in spinal cord injury (SCI) recovery. It explores how manipulating the expression of this RNA affects nerve regeneration and functional outcomes after SCI. The research involves in vitro experiments using PC12 cells, a neuron-like cell line, and in vivo experiments using a rat model of SCI. These experiments tested the impact of increasing (overexpression) or decreasing (knockdown) lncRNA Vof-16 levels. The findings suggest that inhibiting lncRNA Vof-16 expression promotes nerve regeneration and functional recovery after spinal cord injury. This suggests that targeting lncRNA Vof-16 could be a potential therapeutic strategy for SCI.

Study Duration

8 weeks

Participants

102 adult, female, specific-pathogen-free, Sprague-Dawley rats

Evidence Level

Not specified

Key Findings

1
LncRNA Vof-16 overexpression decreases neuronal viability, proliferation, migration and neurite extension in vitro, whereas lncRNA Vof-16 knockdown has the opposite effects.
2
LncRNA Vof-16 is upregulated after spinal cord injury in rats. Knockdown of LncRNA Vof-16 expression in rats after SCI promotes neuron survival and neurogenesis.
3
Knockdown of lncRNA Vof-16 promotes functional recovery in the rat SCI model, with improved BBB scores compared to controls.

Research Summary

This study investigated the role of lncRNA Vof-16 in spinal cord injury (SCI) by constructing knockdown and overexpression lentiviral vectors and transplanting them into PC12 cells and SCI model rats. Results showed that lncRNA Vof-16 overexpression decreased neuronal viability, proliferation, migration, and neurite extension in vitro. Conversely, lncRNA Vof-16 knockdown ameliorated these effects and promoted cell migration and neurite extension. In vivo experiments demonstrated that intrathecal injection of lncRNA Vof-16 knockdown lentivirus facilitated neuron survival and neurogenesis post-SCI, and knockdown of lncRNA Vof-16 promoted functional recovery in the rat SCI model.

Practical Implications

Therapeutic Target

LncRNA Vof-16 may represent a novel therapeutic target for promoting nerve regeneration and functional recovery after spinal cord injury.

Inflammation and Apoptosis Regulation

Understanding the role of lncRNA Vof-16 in regulating inflammation and apoptosis could lead to new strategies for modulating the microenvironment after SCI.

Drug Development

Drugs designed to inhibit lncRNA Vof-16 expression could potentially improve outcomes for individuals with SCI.

Study Limitations

1
The precise mechanism through which lncRNA Vof-16 regulates inflammation and apoptosis signaling pathways remains undetermined.
2
SCI is a complex pathophysiological process influenced by many factors, and effective treatments for SCI remain elusive.
3
The correlation between lncRNA Vof-16 and immune cells remains unclear.

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