Recent investigation of microRNAs on chronic pain has developed a breakthrough in neuropathic pain management. In this study, decreased expression of miR-30a-3p was reported using qRT-PCR analysis and loss of miR-30a-3p promoted neuropathic pain progression in sciatic nerve chronic constrictive injury rats through determining the pain threshold. We predicted miR-30a-3p could target E-cadherin transcriptional activator (EP300) via bioinformatics analysis. Meanwhile, we found that brain-derived neurotrophic factor (BDNF) is involved in neuropathic pain. Here, we exhibited that EP300 epigenetically up-regulated BDNF via enhancing acetylated histone H3 and H4 on the promoter. For another, miR-30a-3p was able to modify the level of BDNF and acetylated histone H3 and H4. Loss of miR-30a-3p enhanced EP300 and BDNF colocalization in CCI rats. Subsequently, it was shown that increased EP300 induced neuropathic pain by an enhancement of neuronal BDNF level in vivo. To sum up, it was revealed that epigenetic modification of BDNF promoted neuropathic pain via EP300 induced by miR-30a-3p in CCI rats.

中文翻译：

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BDNF的表观遗传修饰通过miR-30a-3p / EP300轴介导CCI大鼠的神经性疼痛。

microRNA对慢性疼痛的最新研究在神经性疼痛管理方面取得了突破。在这项研究中，使用qRT-PCR分析报道了miR-30a-3p的表达降低，并且通过确定疼痛阈值，miR-30a-3p的缺失促进了坐骨神经慢性缩窄性损伤大鼠的神经性疼痛进展。我们预测miR-30a-3p可以通过生物信息学分析靶向E-cadherin转录激活因子（EP300）。同时，我们发现脑源性神经营养因子（BDNF）与神经性疼痛有关。在这里，我们展示了EP300通过增强启动子上的乙酰化组蛋白H3和H4，表观遗传上调BDNF。另一方面，miR-30a-3p能够修饰BDNF的水平并乙酰化组蛋白H3和H4。miR-30a-3p的缺失增强了CCI大鼠的EP300和BDNF共定位。后来，结果表明，EP300的增加通过体内神经元BDNF水平的增强而诱发神经性疼痛。总之，揭示了BDNF的表观遗传修饰通过miR-30a-3p在CCI大鼠中通过EP300促进了神经性疼痛。