Altered microRNAs expression profiling in mice with diabetic neuropathic pain

• Mice injected with STZ exhibited hyperglycemia and mechanical allodynia.
• Microarray results showed obvious changes in the miRNA expression after DNP in mice.
• The qRT-PCR and microarray results of two miRNAs in DNP tissue were very similar.

Neuropathic pain is one of the most common chronic complications of diabetes mellitus, one hallmark of which is tactile allodynia. However, the molecular mechanisms underlying tactile allodynia are not well understood. It has been demonstrated that microRNAs (miRNAs) are essential regulators of gene expression in the nervous system where they contribute to neuronal plasticity. Thus, in this study, we investigated the differentially expressed microRNAs in the lumbar spinal dorsal horn of streptozotocin (STZ)-induced diabetic neuropathic pain (DNP) mice and vehicle controls. Results from miRNA microarrays showed that 42 miRNAs were significantly altered in DNP spinal cord tissue (P < 0.05, fold change: ⩾2) compared with control sample. Among them, 21 miRNAs were significantly up-regulated while the other 21 down-regulated. Further validation by quantitative real-time polymerase chain reaction (qRT-PCR) indicated that the 2 significant differentially expressed candidate miRNAs (miR-184-5p and miR-190a-5p) in DNP tissue showed the same changes as in the microarray analysis. The bioinformatics analysis revealed that some of the differentially expressed miRNAs after DNP were potential regulators of some inflammation associated with genes that are known to be involved in the pathogenesis of DNP. These findings suggest that aberrant expression of miRNAs may contribute to the pathogenesis of DNP and are potential targets for therapeutic interventions following DNP.