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不同神经病理性疼痛小鼠模型脑区的基因调控网络。

The gene regulatory network in different brain regions of neuropathic pain mouse models.

机构信息

Department of Oncology, The First Hospital of Jiaxing, The First Affiliated Hospital of Jiaxing  University, Jiaxing, China.

出版信息

Eur Rev Med Pharmacol Sci. 2020 May;24(9):5053-5061. doi: 10.26355/eurrev_202005_21198.

Abstract

OBJECTIVE

Neuropathic pain is directly developed from lesions or somatosensory nervous system diseases that are associated with emotion regulation. In general population, the incidence of neuropathic pain ranges from 7% to 10%, but the underlying mechanism remains largely unknown. Neuropathic pain is often associated with structural and functional abnormalities in multiple brain regions, and its regulation has been shown to correspond with the forebrain, including nucleus accumbens (NAc), medial prefrontal cortex (mPFC) and periaqueductal gray (PAG).

MATERIALS AND METHODS

To investigate the molecular mechanism of neuropathic pain across different brain regions, we identified the differentially expressed genes (DEGs) between the spared nerve injury model (SNI) mice suffering neuropathic pain and the control Sham mice in NAc, mPFC and PAG three brain regions, and mapped these genes onto a comprehensively functional association network. Thereafter, novel neuropathic pain genes in these three regions were identified using With Random Walk with Restart (RWR) analysis, such as Asic3, Cd200r1 and MT2, besides well-known Capn11 and CYP2E1.

RESULTS

Interactions or cross talks among DEGs in NAc, mPFC and PAG three brain regions were discovered.

CONCLUSIONS

Our results provide novel insights into neuropathic pain and help to explore therapeutic targets in the treatment.

摘要

目的

神经病理性疼痛是直接由病变或躯体感觉神经系统疾病引起的,与情绪调节有关。在一般人群中,神经病理性疼痛的发病率为 7%至 10%,但其潜在机制在很大程度上尚不清楚。神经病理性疼痛通常与多个脑区的结构和功能异常有关,其调节作用已被证明与前脑有关,包括伏隔核(NAc)、内侧前额叶皮层(mPFC)和导水管周围灰质(PAG)。

材料和方法

为了研究不同脑区神经病理性疼痛的分子机制,我们鉴定了在 spared nerve injury 模型(SNI)小鼠神经病理性疼痛和对照 Sham 小鼠的 NAc、mPFC 和 PAG 三个脑区之间差异表达的基因(DEGs),并将这些基因映射到一个全面的功能关联网络中。此后,我们使用随机游走重启(RWR)分析在这三个区域中鉴定出了新的神经病理性疼痛基因,如 Asic3、Cd200r1 和 MT2,以及众所周知的 Capn11 和 CYP2E1。

结果

发现了 NAc、mPFC 和 PAG 三个脑区之间的 DEGs 相互作用或串扰。

结论

我们的结果为神经病理性疼痛提供了新的见解,并有助于探索治疗中的治疗靶点。

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