The role of epogenetic modulation in the neuropathic pain

疼痛是人类最不舒服的感觉之一，但其发生机制尚不清楚，本研究以表观遗传修饰为重点进行研究。我们针对脑源性神经营养因子（BDNF）基因构建的独特性，对不同剪接变体进行mRNA定量、CpG岛甲基化分析和组蛋白修饰。许多CpG岛甲基化率变化很小，但在神经损伤大鼠中显著高于幼稚大鼠、幼稚大鼠和假手术大鼠。部分外显子启动子区甲基化的树状图表明，神经损伤大鼠和未损伤对照组在第一分支的分类完全符合条件。这些被认为是未来神经病理性疼痛生物标志物的强有力的候选者。

Pain is one of the most uncomfortable feeling to have of humans, but the mechanism is unclear.In this study, we conducted research by focusing on the epigenetic modification. We focused on the unique feature of brain-derived neurotrophic factor(BDNF)gene construction, we performed the mRNA quantification of the various splice variants, methylation analysis of CpG islands of each splice variant, and histone modification. Many CpG islands methylation rates changes were very little but significantly higher in nerve-injured rats than naive, or naive and sham rats. The dendrogram from methylation profiles of some exon's promoter region demonstrated that classification of nerve injured rats and naive controls at the first branch completely matched the condition. These were considered to be strong candidates for biomarkers of neuropathic pain in the future.