Transcriptome analysis of trigeminal ganglia following masseter muscle inflammation in rats.
Transcriptome analysis of trigeminal ganglia following masseter muscle inflammation in rats.
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DOI：
10.1177/1744806916668526
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发表时间：
2016
期刊：
影响因子：
3.3
通讯作者：
Ro JY
中科院分区：
文献类型：
--
作者：
Chung MK;Park J;Asgar J;Ro JY
咀嚼肌肉的慢性疼痛是一个主要的医学问题。虽然咀嚼肌持续疼痛的机制还不完全清楚，但肌肉炎症或损伤后伤害性初级传入的敏化有助于肌肉痛觉过敏。众所周知，颅面肌损伤或炎症诱导三叉神经节中多个基因的调节，这与肌肉痛觉过敏有关。然而，咬肌炎症后三叉神经节内的整体转录谱尚未确定。在本研究中，我们对大鼠三叉神经节进行了RNA测序分析，以确定与大鼠咬肌炎症后痛觉过敏相关基因的转录组谱。咬肌炎症在三叉神经节中的差异调节基因>；3500。主要的生物通路被预测与三叉神经节内驻留的非神经细胞的激活或免疫细胞的募集有关。为了重点分析与伤害性感受器更相关的基因，我们选择了与疼痛机制有关的基因，富含中小型感觉神经元的基因，以及富含TRPV1系伤害性感受器的基因。在2320个候选基因中，有622个基因在咬肌炎症后表现出差异表达。当分析局限于这些候选基因时，与G蛋白偶联信号和突触可塑性相关的通路被预测为丰富。对单个基因表达变化的检测证实了与咬肌痛觉过敏相关的多个伤害性感受器基因(例如TRPV1、TRPA1、P2rx3、Tac1和BDNF)的转录变化，并提出了一些新的可能贡献基因(例如Piezo2、Tem100和Hdac9)。这些发现将进一步促进我们对持续性颅面部肌肉疼痛状况所涉及的外周机制的理解，并为识别潜在靶向治疗此类状况的新基因或基因集提供合理的基础。
Chronic pain in masticatory muscles is a major medical problem. Although mechanisms underlying persistent pain in masticatory muscles are not fully understood, sensitization of nociceptive primary afferents following muscle inflammation or injury contributes to muscle hyperalgesia. It is well known that craniofacial muscle injury or inflammation induces regulation of multiple genes in trigeminal ganglia, which is associated with muscle hyperalgesia. However, overall transcriptional profiles within trigeminal ganglia following masseter inflammation have not yet been determined. In the present study, we performed RNA sequencing assay in rat trigeminal ganglia to identify transcriptome profiles of genes relevant to hyperalgesia following inflammation of the rat masseter muscle. Masseter inflammation differentially regulated >3500 genes in trigeminal ganglia. Predominant biological pathways were predicted to be related with activation of resident non-neuronal cells within trigeminal ganglia or recruitment of immune cells. To focus our analysis on the genes more relevant to nociceptors, we selected genes implicated in pain mechanisms, genes enriched in small- to medium-sized sensory neurons, and genes enriched in TRPV1-lineage nociceptors. Among the 2320 candidate genes, 622 genes showed differential expression following masseter inflammation. When the analysis was limited to these candidate genes, pathways related with G protein-coupled signaling and synaptic plasticity were predicted to be enriched. Inspection of individual gene expression changes confirmed the transcriptional changes of multiple nociceptor genes associated with masseter hyperalgesia (e.g., Trpv1, Trpa1, P2rx3, Tac1, and Bdnf) and also suggested a number of novel probable contributors (e.g., Piezo2, Tmem100, and Hdac9). These findings should further advance our understanding of peripheral mechanisms involved in persistent craniofacial muscle pain conditions and provide a rational basis for identifying novel genes or sets of genes that can be potentially targeted for treating such conditions.
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影响因子：
3.3
作者：
Simonic-Kocijan S;Zhao X;Liu W;Wu Y;Uhac I;Wang K
通讯作者：
Wang K
DOI：
10.1016/j.jpain.2014.09.010
发表时间：
2014-12
期刊：
The journal of pain
影响因子：
--
作者：
Goswami SC;Mishra SK;Maric D;Kaszas K;Gonnella GL;Clokie SJ;Kominsky HD;Gross JR;Keller JM;Mannes AJ;Hoon MA;Iadarola MJ
通讯作者：
Iadarola MJ
影响因子：
7.4
作者：
Ambalavanar, R;Moritani, M;Dessem, D
通讯作者：
Dessem, D
影响因子：
14.9
作者：
Mi H;Poudel S;Muruganujan A;Casagrande JT;Thomas PD
通讯作者：
Thomas PD
影响因子：
3.3
作者：
Salerno, K. M.;Jing, X.;Diges, C. M.;Davis, B. M.;Albers, K. M.
通讯作者：
Albers, K. M.