Nogo-A promotes inflammatory heat hyperalgesia by maintaining TRPV-1 function in the rat dorsal root ganglion neuron

被引:17
作者
Hu, Fang [1 ,2 ]
Liu, Huai-Cun [3 ]
Su, Dong-Qiang [3 ]
Chen, Hai-Jing [1 ]
Chan, Sun-On [4 ]
Wang, Yun [1 ,5 ]
Wang, Jun [3 ]
机构
[1] Peking Univ, Hlth Sci Ctr,Dept Neurobiol, Natl Hlth Commiss,Neurosci Res Inst, Key Lab Neurosci,Minist Educ & Neurosci, Beijing, Peoples R China
[2] Qingdao Univ, Sch Pharm, Dept Pharmacol, Qingdao, Peoples R China
[3] Peking Univ, Sch Basic Med Sci, Dept Anat & Histol, 38 Xueyuan Rd, Beijing 100083, Peoples R China
[4] Chinese Univ Hong Kong, Fac Med, Sch Biomed Sci, Hong Kong, Peoples R China
[5] Peking Univ, McGovern Inst Brain Res, Peking Univ Int Data Grp PKU IDG, Beijing, Peoples R China
基金
中国国家自然科学基金; 北京市自然科学基金;
关键词
RTN4A; inflammatory pain; cytoskeleton; PRIMARY SENSORY NEURONS; NEURITE OUTGROWTH INHIBITOR; MYELIN-ASSOCIATED INHIBITOR; AXON REGENERATION; MESSENGER-RNA; MICE LACKING; SPINAL-CORD; RECEPTOR; PROTEIN; KINASE;
D O I
10.1096/fj.201800382RR
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Nogo-A is a key inhibitory molecule of axon regeneration in oligodendrocytes. However, little is known about its role in adult neurons. In this study, we showed an important function of Nogo-A on regulation of inflammatory pain in dorsal root ganglion (DRG) neurons. In adult rats with complete Freund's adjuvant (CFA) hind paw inflammation, DRG neurons showed a significant increase in Nogo-A expression. Disruption of Nogo-A signaling with Nogo-66 receptor antagonist peptide, Nogo-A blocking antibody, Nogo-A short hairpin RNA, or Nogo-A gene knockout attenuated CFA-induced inflammatory heat hyperalgesia. Moreover, disruption of Nogo-A signaling suppressed the function and expression in DRG neurons of the transient receptor potential vanilloid subfamily member (TRPV)-1 channel, which is known to be the endogenous transducer of noxious heat during inflammation. These effects were accompanied with a reduction in LIM domain kinase (LIMK)/cofilin phosphorylation and actin polymerization. Similar disruption of actin filament architecture by direct action of Latrunculin A reduced the TRPV-1 activity and up-regulation of TRPV-1 protein caused by CFA. We conclude that Nogo-A plays an essential role in the development of inflammatory heat hyperalgesia, partly through maintaining TRPV-1 function via activation of the LIMK/cofilin pathway, which regulates actin filament dynamics. These findings support a therapeutic potential of modulating Nogo-A signaling in pain management.Hu, F., Liu, H.-C., Su, D.-Q., Chen, H.-J., Chan, S.-O., Wang, Y., Wang, J. Nogo-A promotes inflammatory heat hyperalgesia by maintaining TRPV-1 function in the rat dorsal root ganglion neuron.
引用
收藏
页码:668 / 682
页数:15
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