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Published on: February 22, 2019
Differential expression of microRNAs in mouse pain models
Ricardo Kusuda1, Flaviane Cadetti, Maria I Ravanelli
1Department of Physiology, Ribeirão Preto School of Medicine, University of São Paulo, Ribeirão Preto, Brazil.
Background:
MicroRNAs (miRNAs) are short non-coding RNAs that inhibit translation of target genes by binding to their mRNAs. The expression of numerous brain-specific miRNAs with a high degree of temporal and spatial specificity suggests that miRNAs play an important role in gene regulation in health and disease. Here we investigate the time course gene expression profile of miR-1, -16, and -206 in mouse dorsal root ganglion (DRG), and spinal cord dorsal horn under inflammatory and neuropathic pain conditions as well as following acute noxious stimulation.
Results:
Quantitative real-time polymerase chain reaction analyses showed that the mature form of miR-1, -16 and -206, is expressed in DRG and the dorsal horn of the spinal cord. Moreover, CFA-induced inflammation significantly reduced miRs-1 and -16 expression in DRG whereas miR-206 was downregulated in a time dependent manner. Conversely, in the spinal dorsal horn all three miRNAs monitored were upregulated. After sciatic nerve partial ligation, miR-1 and -206 were downregulated in DRG with no change in the spinal dorsal horn. On the other hand, axotomy increases the relative expression of miR-1, -16, and 206 in a time-dependent fashion while in the dorsal horn there was a significant downregulation of miR-1. Acute noxious stimulation with capsaicin also increased the expression of miR-1 and -16 in DRG cells but, on the other hand, in the spinal dorsal horn only a high dose of capsaicin was able to downregulate miR-206 expression.
Conclusions:
Our results indicate that miRNAs may participate in the regulatory mechanisms of genes associated with the pathophysiology of chronic pain as well as the nociceptive processing following acute noxious stimulation. We found substantial evidence that miRNAs are differentially regulated in DRG and the dorsal horn of the spinal cord under different pain states. Therefore, miRNA expression in the nociceptive system shows not only temporal and spatial specificity but is also stimulus-dependent.
Insights
MicroRNAs (miRNAs) are differentially regulated in the nervous system during pain. Their expression in the dorsal root ganglion and spinal cord changes based on pain type and stimulus, indicating a role in pain regulation.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) are key regulators of gene expression.
- Brain-specific miRNAs exhibit temporal and spatial specificity, suggesting crucial roles in neural function.
- Dysregulation of miRNAs is implicated in various diseases, including neurological disorders.
Purpose of the Study:
- To investigate the time-course gene expression of miR-1, -16, and -206.
- To analyze miRNA expression in the mouse dorsal root ganglion (DRG) and spinal cord dorsal horn.
- To determine miRNA regulation under inflammatory, neuropathic pain, and acute noxious stimulation conditions.
Main Methods:
- Quantitative real-time polymerase chain reaction (qRT-PCR) was used.
- Expression levels of mature miR-1, -16, and -206 were quantified.
- Pain models included Complete Freund's Adjuvant (CFA)-induced inflammation, sciatic nerve partial ligation, axotomy, and capsaicin stimulation.
Main Results:
- miR-1, -16, and -206 are expressed in DRG and spinal cord dorsal horn.
- Inflammation (CFA) downregulated miR-1 and -16 in DRG; miR-206 was time-dependently downregulated.
- Neuropathic pain (nerve ligation/axotomy) and capsaicin stimulation induced varied miRNA expression changes in DRG and spinal cord.
Conclusions:
- miRNAs are differentially regulated in the DRG and spinal cord dorsal horn under various pain states.
- miRNA expression is stimulus-dependent and exhibits temporal and spatial specificity in the nociceptive system.
- miRNAs likely participate in the gene regulatory mechanisms underlying chronic pain pathophysiology and acute nociceptive processing.
