College of life Science, Inner Mongolia Agricultural University, No. 306 Zhaowuda Road, Saihan District, Hohhot, 010018, People's Republic of China.
College of Basic Medicine, Inner Mongolia Medical University, Hohhot, 010110, People's Republic of China.
Biol Res. 2018 Aug 17;51(1):25. doi: 10.1186/s40659-018-0174-7.
This aim of this study was to investigate the key genes and pathways involved in the response to pain in goat and sheep by transcriptome sequencing.
Chronic pain was induced with the injection of the complete Freund's adjuvant (CFA) in sheep and goats. The animals were divided into four groups: CFA-treated sheep, control sheep, CFA-treated goat, and control goat groups (n = 3 in each group). The dorsal root ganglions of these animals were isolated and used for the construction of a cDNA library and transcriptome sequencing. Differentially expressed genes (DEGs) were identified in CFA-induced sheep and goats and gene ontology (GO) enrichment analysis was performed.
In total, 1748 and 2441 DEGs were identified in CFA-treated goat and sheep, respectively. The DEGs identified in CFA-treated goats, such as C-C motif chemokine ligand 27 (CCL27), glutamate receptor 2 (GRIA2), and sodium voltage-gated channel alpha subunit 3 (SCN3A), were mainly enriched in GO functions associated with N-methyl-D-aspartate (NMDA) receptor, inflammatory response, and immune response. The DEGs identified in CFA-treated sheep, such as gamma-aminobutyric acid (GABA)-related DEGs (gamma-aminobutyric acid type A receptor gamma 3 subunit [GABRG3], GABRB2, and GABRB1), SCN9A, and transient receptor potential cation channel subfamily V member 1 (TRPV1), were mainly enriched in GO functions related to neuroactive ligand-receptor interaction, NMDA receptor, and defense response.
Our data indicate that NMDA receptor, inflammatory response, and immune response as well as key DEGs such as CCL27, GRIA2, and SCN3A may regulate the process of pain response during chronic pain in goats. Neuroactive ligand-receptor interaction and NMDA receptor as well as GABA-related DEGs, SCN9A, and TRPV1 may modulate the process of response to pain in sheep. These DEGs may serve as drug targets for preventing chronic pain.
本研究旨在通过转录组测序探讨羊慢性痛反应相关的关键基因和通路。
采用完全弗氏佐剂（CFA）对羊和山羊进行慢性痛诱导。将动物分为 4 组：CFA 处理羊组、对照羊组、CFA 处理山羊组和对照山羊组（每组 3 只）。分离这些动物的背根神经节，构建 cDNA 文库并进行转录组测序。鉴定 CFA 诱导的羊和山羊中的差异表达基因（DEGs），并进行基因本体（GO）富集分析。
共鉴定出 CFA 处理山羊和绵羊中的 1748 个和 2441 个 DEGs。在 CFA 处理山羊中鉴定出的 DEGs，如 C-C 基序趋化因子配体 27（CCL27）、谷氨酸受体 2（GRIA2）和电压门控钠离子通道 α 亚基 3（SCN3A），主要富集于 N-甲基-D-天冬氨酸（NMDA）受体、炎症反应和免疫反应相关的 GO 功能。在 CFA 处理绵羊中鉴定出的 DEGs，如γ-氨基丁酸（GABA）相关的 DEGs（GABA-A 型受体 γ3 亚基[GABRG3]、GABRB2 和 GABRB1）、SCN9A 和瞬时受体电位阳离子通道亚家族 V 成员 1（TRPV1），主要富集于神经活性配体-受体相互作用、NMDA 受体和防御反应相关的 GO 功能。
本研究数据表明，NMDA 受体、炎症反应和免疫反应以及关键 DEGs（如 CCL27、GRIA2 和 SCN3A）可能调节山羊慢性痛反应过程。神经活性配体-受体相互作用和 NMDA 受体以及 GABA 相关的 DEGs、SCN9A 和 TRPV1 可能调节绵羊对疼痛的反应过程。这些 DEGs 可能成为预防慢性疼痛的药物靶点。
