RNA-seq分析揭示了干扰素调节因子4基因敲除小鼠慢性压迫性损伤诱发神经病理性疼痛的相关基因。

Jiayi Peng, Yunlin Wu, Qi E, Ziyin Zhou, Xianjie Wen
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摘要

目的通过对小鼠脊髓进行RNA-seq分析,探讨野生型慢性压迫性损伤(CCI)小鼠(WT-CCI)与干扰素调节因子4(IRF4)敲除CCI小鼠(KO-CCI)之间基因表达的差异:方法:对慢性坐骨神经结扎小鼠的脊髓组织进行RNA-seq分析,并使用基因本体和京都基因与基因组百科全书进行分析:结果:与野生型CCI(WT-CCI)组相比,IRF4基因敲除(KO-CCI)组小鼠脊髓中共有104个基因上调,116个基因下调。KO-CCI小鼠的生物过程组中有1472个差异表达基因,细胞组分组中有62个差异表达基因,分子功能组中有163个差异表达基因。共有 14 个与炎症反应相关的基因有差异表达。实时 PCR 结果证实,在 KO-CCI 组中,Pparg 和 Grpr mRNA 表达上调,Arg 1 和 Ccl11 mRNA 表达下调:IRF4可能通过调控Grpr、Mas1、Galr3、Nos2、Arg1、Ccl11、Ptgs2、S100a8、Pparg、Cd40、Has2、Gpr151、Il123a、Capns2、Ankrd1、Ccnb1和Nppb基因参与神经病理性疼痛。
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RNA-seq analysis revealed genes associated with neuropathic pain induced by chronic compressive injury in interferon regulatory factors 4 knockout mice.

Objective: To explore the differential expression of genes between wild-type chronic compressive injury (CCI) mice (WT-CCI) and interferon regulatory factors 4 (IRF4) knockout CCI mice (KO-CCI) by RNA-seq analysis of the mouse spinal cord.

Methods: RNA-seq analysis of the spinal cord tissue of the chronic sciatic nerve ligation mice and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses were used.

Results: A total of 104 genes were up-regulated and 116 genes were down-regulated in spinal cord of the mice in IRF4 knockout (KO-CCI) group compared with that in the wild-type CCI (WT-CCI) group. There were 1472 differentially expressed genes in the biological process group, 62 differentially expressed genes in the cellular component group, and 163 differentially expressed genes in the molecular function group in KO-CCI mice. A total of 14 genes related to inflammatory reactions were differentially expressed. Real-time PCR results confirmed that Pparg and Grpr mRNA expression was up-regulated and Arg 1 and Ccl11 mRNA expression was down-regulated in the KO-CCI group.

Conclusion: IRF4 is involved in neuropathic pain in CCI mice, IRF4 may participate in neuropathic pain by regulating Grpr, Mas1, Galr3, Nos2, Arg1, Ccl11, Ptgs2, S100a8, Pparg, Cd40, Has2, Gpr151, Il123a, Capns2, Ankrd1, Ccnb1, and Nppb genes.

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