Cycling Exercise Affects the Expression of Apoptosis-Associated microRNAs after Spinal Cord Injury in Rats

Exp Neurol, 2010 · DOI: 10.1016/j.expneurol.2010.08.032 · Published: November 1, 2010

Simple Explanation

Spinal cord injuries (SCI) cause primary mechanical trauma and secondary damage from inflammation and cell death. MicroRNAs (miRs) regulate gene expression and are involved in cell proliferation and death. This study examines how miRs and their targets in apoptosis are affected by SCI and how cycling exercise influences miR expression. The study found that SCI increased miR Let-7a and miR16, while exercise increased miR21 and decreased miR15b. These changes correlated with target gene expression: decreased pro-apoptotic (PTEN, PDCD4, RAS mRNA) and increased anti-apoptotic (Bcl-2 mRNA) genes. The study suggests that exercise may benefit SCI recovery by affecting multiple miRs and their targets, regulating apoptosis after SCI. This might protect nerve cells and/or help them regenerate.

Study Duration

10 and 31 days

Participants

Adult female Sprague-Dawley rats (n=6 for each of 5 groups)

Evidence Level

Not specified

Key Findings

1
SCI results in increased expression of miR Let-7a and miR16.
2
Exercise leads to elevated levels of miR21 and decreased levels of miR15b.
3
Changes in miR expression are correlated with changes in expression of their target genes: pro-apoptotic (decreased PTEN, PDCD4 and RAS mRNA) and anti-apoptotic (increased Bcl-2 mRNA) target genes.

Research Summary

This study investigates the effects of cycling exercise on the expression of apoptosis-associated microRNAs (miRs) after spinal cord injury (SCI) in rats. SCI leads to increased expression of pro-apoptotic miRs, while exercise influences the expression of miRs and their target genes involved in apoptotic pathways. The results show that SCI increases the expression of miR Let-7a and miR16, while exercise elevates miR21 levels and decreases miR15b levels. These changes in miR expression are correlated with changes in the expression of their target genes, including pro-apoptotic and anti-apoptotic genes. The study suggests that exercise may have beneficial effects on SCI by influencing multiple miRs and their targets, contributing to the functional regulation of apoptosis. This highlights a potential neuroprotective effect of exercise through modulation of miR expression and subsequent regulation of apoptosis.

Practical Implications

Therapeutic Potential

Cycling exercise can potentially be used as a therapeutic intervention to modulate miR expression and reduce apoptosis after SCI.

Neuroprotective Mechanism

The study identifies a potential neuroprotective mechanism of exercise through the regulation of miRs and their target genes involved in apoptotic pathways.

Targeted Therapies

The identified miRs and their target genes could be potential targets for developing novel therapeutic strategies to promote recovery after SCI.

Study Limitations

1
Further studies are needed to establish a direct effect of miR inhibition on apoptosis after SCI using pharmacological and/or antisense knockdown.
2
The study focused on a complete transection injury model, and the results may not be directly applicable to other types of SCI.
3
The long term effects of exercise on miR expression were not observed, further research is needed to identify the optimal duration and intensity of exercise for sustained benefits.

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