Changes in microRNA expression in the brachial plexus avulsion model of neuropathic pain

Abstract

Abstract. The present study aimed to perform microRNA (miRNA/miR) expression profiling of the thalamus (T), the anterior cingulate (Ac), the dorsal horn of the spinal cord (dHSc) and the blood (B) in post-complete brachial plexus avulsion (cBPA) pain model, and analyze biological functions. Neuropathic pain was induced in Sprague-dawley rats by cBPA. Animal behavioral tests were performed to differentiate the pain and control groups. dHSc, T, Ac and B tissues were collected from the two groups for miRNA array analysis. The predicted mRNA targets were investigated by Gene Ontology analysis and pathway analysis. The results revealed that in the post-cBPA pain model, there were 10 differentially expressed miRNAs revealed among 4 different tissues. A total of 4 microRNAs in the Ac and 3 microRNAs in the T were shown to be significantly upregulated. The functions of the differentially expressed miRNAs in the Ac and T were synergetic in the aspect of positive regulation of neuron apoptotic process, inhibition of long-term potentiation and formation of synapse plasticity. miR-30c-1-3p and its predicted genes [calcium/calmodulin dependent protein kinase IIβ (Camk2b) and protein kinase Cγ (Prkcg)] existed in the AC and T groups with significant changes in expression. There were 2 miRNAs in the dHSc and B groups, respectively, with significant downregulation. The function of the change in miRNAs in the dHSc group was opposite to that in the Ac and T groups. The differentially expressed microRNAs in the B group were revealed to be negative for the regulation of cell apoptosis. In conclusion, the central nerve groups (Ac and T) and the peripheral nerve group (dHSc) exhibited contrasting effects on synapse plasticity and neuron apoptosis. miR-30c-1-3p and its predicted genes (camk2b and Prkcg) existed in the AC and T groups with significant changes in expression.

Microarray analysis of potential biomarkers of brachial plexus avulsion caused neuropathic pain in male rat

“…Neuropathy rats frequently responded with a withdrawal that was exaggerated in amplitude and duration. The withdrawal responses were assessed on a scale of 3–0 points: 3 points, a vigorous response in which the rat licked the paw; 2 points, a response in which the paw has elevated the paw; 1 point, a response in which the paw had little or no weight born on it and 0 points, the paw was not moved [ 5 ].…”

Microarray Analysis of Potential Biomarkers for brachial plexus avulsion caused neuropathic pain

“…Neuropathy rats frequently responded with a withdrawal that was clearly exaggerated in amplitude and duration. The withdrawal responses were assessed on a scale of 3-0 points: 3 points, a vigorous response in which the rat licked the paw; 2 points, a response in which the paw has elevated the paw; 1 point, a response in which the paw had little or no weight born on it and 0 points, the paw was not moved [5].…”

Comparison of Different In Vivo Animal Models of Brachial Plexus Avulsion and Its Application in Pain Study

“…Similar work has been done by Kobayashi et al [ 30 ] on the application of the p75NTR inhibitory antibody and Zhao and Wu [ 31 ] on histone deacetylase inhibition to suppress neuropathic pain after BPA. Recent work on level changes of microRNA could supply other new ideas in BPA-induced neuropathic pain treatment [ 32 ], and enhancer of zeste homolog 2 (EZH2) was proven to be a novel regulator of neuroinflammation and neuropathic pain via the mTOR signaling pathway in the anterior cingulate cortex, which could be another target of pain treatment [ 33 ]. In other words, an anterior approach BPA model of mice or rats at any trunk of the brachial plexus could be implemented and become a good model of related research, especially on the research in the neuropathic pain field.…”

“…Therapeutic strategies for the treatment of neuropathic pain are always limited by its elusive mechanisms and the incomplete understanding of nervous system plasticity after the initial injury [ 79 ], so we still need to search for different targets to treat this pain. Researches targeting the gene level have emerged with the development of genomics, and the results of the preliminary investigations seemed promising based on BPA models [ 32 , 33 , 44 ], which may be another novel route of the BPA treatment.…”