TET1 Participates in Complete Freund’s Adjuvant-induced Trigeminal Inflammatory Pain by Regulating Kv7.2 in a Mouse Model  

作　　者：Dengcheng Zhan Jingjing Zhang Songxue Su Xiuhua Ren Sen Zhao Weidong Zang Jing Cao 

机构地区：[1]Department of Human Anatomy,School of Basic Medical Sciences,Zhengzhou University,Zhengzhou,450001,China [2]Neuroscience Research Institute,Zhengzhou University,Zhengzhou,450001,China

出　　处：《Neuroscience Bulletin》2024年第6期707-718,共12页神经科学通报（英文版）

基　　金：supported by the National Natural Science Foundation of China(81771195 and 81971061);the Program for Innovative Research Team in Universities of Henan Province(22IRTSTHN028).

摘　　要：Trigeminal inflammatory pain is one of the most severe pain-related disorders in humans;however,the underlying mechanisms remain largely unknown.In this study,we investigated the possible contribution of interaction between ten-eleven translocation methylcytosine dioxygenase 1(TET1)and the voltage-gated K^(+)channel Kv7.2(encoded by Kcnq2)to orofacial inflammatory pain in mice.We found that complete Freund’s adjuvant(CFA)injection reduced the expression of Kcnq2/Kv7.2 in the trigeminal ganglion(TG)and induced orofacial inflammatory pain.The involvement of Kv7.2 in CFA-induced orofacial pain was further confirmed by Kv7.2 knockdown or overexpression.Moreover,TET1 knockdown in Tet1^(flox/flox)mice significantly reduced the expression of Kv7.2 and M currents in the TG and led to pain-like behaviors.Conversely,TET1 overexpression by lentivirus rescued the CFA-induced decreases of Kcnq2 and M currents and alleviated mechanical allodynia.Our data suggest that TET1 is implicated in CFA-induced trigeminal inflammatory pain by positively regulating Kv7.2 in TG neurons.

关 键 词：Facial pain KCNQ2 potassium channel TET1 protein 

分 类 号：R402[医药卫生—临床医学] R-332