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A Neurosphere Assay to Evaluate Endogenous Neural Stem Cell Activation in a Mouse Model of Minimal Spinal Cord Injury
Published on: September 13, 2018
MiRNA-411 attenuates inflammatory damage and apoptosis following spinal cord injury
1General Hospital of Heilongjiang General Administration of Agriculture and Reclamation, Haerbin, China. 13501772762@126.com.
Objective:
To investigate the role and regulate the target of miRNA-411 on spinal cord injury.
Materials And Methods:
The microglia cultured in vitro was activated by lipopolysaccharide (LPS) to express the inflammatory phenotype. The inflammatory response through miRNA-411 transfection in microglia was measured to certain whether increased miRNA-411 suppressed interleukin-18 (IL-18) level to attenuate the inflammation amplification via downregulating JNK pathway. Furthermore, we established spinal cord injury (SCI) model in SD rats and further explored the glial inflammatory degree and neurological recovery following miRNA-411 treatment. Lastly, we estimated the hindlimbs function of SCI rats with miRNA-411 administration or not within four weeks at post-SCI.
Results:
In vitro, miRNA-411 inhibited IL-18 expression and downregulated JNK pathway, along with that inflammatory microglia were declined. In SCI rats, we detected the decreased amounts of inflammatory microglia and reduction of the inflammatory factors after miRNA-411 treatment. IL-18 and JNK pathway was also restrained resulted from increased miRNA-411. In addition, apoptosis degree in injury site reduced and survived axons were relatively multiple in the miRNA-411 group compared with the SCI group. The Basso-Beattie-Bresnahan (BBB) locomotor scores of miRNA-411 treated rats were superior to those in rats with no treatment.
Conclusions:
MiRNA-411 increase ameliorates the inflammatory microglia-induced neurological lesion and promotes neural recovery by JNK pathway inhibition via negative targeting IL-18 in SCI.
Insights
Increasing microRNA-411 (miRNA-411) reduces inflammation and promotes neural recovery after spinal cord injury (SCI). This study shows miRNA-411 suppresses interleukin-18 (IL-18) and the JNK pathway, improving hindlimb function in SCI rats.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- Spinal cord injury (SCI) triggers neuroinflammation mediated by microglia.
- MicroRNA-411 (miRNA-411) has potential regulatory roles in inflammatory processes.
- Interleukin-18 (IL-18) and the JNK pathway are key mediators of inflammation in SCI.
Purpose of the Study:
- To investigate the role of miRNA-411 in spinal cord injury.
- To determine if miRNA-411 can regulate interleukin-18 (IL-18) and the JNK pathway.
- To evaluate the therapeutic potential of miRNA-411 for promoting neurological recovery after SCI.
Main Methods:
- In vitro studies using lipopolysaccharide (LPS)-activated microglia to assess miRNA-411 effects on inflammation.
- Establishment of an SCI rat model to evaluate glial inflammatory response and neurological recovery.
- Assessment of hindlimb locomotor function using the Basso-Beattie-Bresnahan (BBB) scale.
Main Results:
- In vitro, miRNA-411 transfection inhibited IL-18 expression and downregulated the JNK pathway, reducing inflammatory microglia.
- In SCI rats, miRNA-411 treatment decreased inflammatory microglia, inflammatory factors, IL-18, and JNK pathway activation.
- miRNA-411 administration led to reduced apoptosis, increased axon survival, and improved BBB scores in SCI rats.
Conclusions:
- Increased miRNA-411 ameliorates neuroinflammation and neurological damage in spinal cord injury.
- miRNA-411 promotes neural recovery by inhibiting the JNK pathway through negative targeting of IL-18.
- miRNA-411 represents a potential therapeutic strategy for spinal cord injury treatment.
