C/EBPβ Participates in Nerve Trauma-Induced TLR7 Upregulation in Primary Sensory Neurons

被引：7
作者：
He, Long [1 ]
Cao, Jing [2 ]
Jiang, Bao-Chun [3 ]
Yang, Jian-Jun [1 ]
Tao, Yuan-Xiang [4 ]
Ai, Yanqiu [1 ]
机构：
[1] Zhengzhou Univ, Dept Anesthesiol Pain & Perioperat Med, Affiliated Hosp 1, Zhengzhou 450052, Henan, Peoples R China
[2] Zhengzhou Univ, Coll Basic Med, Dept Anat, Zhengzhou 450001, Henan, Peoples R China
[3] Nantong Univ, Inst Pain Med & Special Environm Med, Nantong 226019, Jiangsu, Peoples R China
[4] Rutgers State Univ, New Jersey Med Sch, Dept Anesthesiol, Newark, NJ 07103 USA
来源：
MOLECULAR NEUROBIOLOGY | 2022年 / 59卷 / 04期
基金：
中国国家自然科学基金;
关键词：
TLR7; C/EBP beta; Dorsal root ganglion; Nerve trauma; Neuropathic pain; NEUROPATHIC PAIN; CONTRIBUTES; RECEPTOR; TRANSCRIPTION; RECOGNITION; RAT;
D O I：
10.1007/s12035-022-02763-0
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Nerve trauma-induced toll-like receptor 7 (TLR7) expression level increases in primary sensory neurons in injured dorsal root ganglion (DRG) avails to neuropathic pain, but the reason is still unknown. In the current study, we showed that unilateral lumbar 4 (L4) spinal nerve ligation (SNL) upregulated CCAAT/enhancer-binding protein-beta (C/EBP beta) expression in ipsilateral L4 DRG. Preventing this elevation attenuated the SNL-induced upregulation of TLR7 in the ipsilateral L4 DRG and inhibited cold/thermal hyperalgesia and mechanical allodynia. In injected DRG, mimicking nerve trauma-induced C/EBPP upregulation increased TLR7 levels, augmented responses to cold/thermal/mechanical stimuli, and caused ipsilateral spontaneous pain with no SNL. Mechanistically, SNL upregulated binding of increased C/EBP beta to T1r7 promoter in ipsilateral L4 DRG. Accorded that C/EBP beta could trigger the activation of T1r7 promoter and co-expressed with T1r7 mRNA in individual DRG neurons, our findings strongly suggest the role of C/EBP beta in nerve trauma-mediated TLR7 upregulation in injured primary sensory neurons.
引用
收藏
页码：2629 / 2641
页数：13
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