Open AccessHistone methylation-mediated microRNA-32-5p down-regulation in sensory neurons regulates pain behaviors via targeting Cav3.2 channels
Author(s) -
Renfei Qi,
Junping Cao,
Yufang Sun,
Yanping Li,
Zitong Huang,
Dongsheng Jiang,
Xinghong Jiang,
Terrance P. Snutch,
Yuan Zhang,
Jin Tao
Publication year - 2022
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2117209119
Subject(s) - neuropathic pain , microrna , trigeminal ganglion , histone , epigenetics , allodynia , chemistry , medicine , microbiology and biotechnology , pharmacology , biology , nociception , neuroscience , receptor , sensory system , gene , hyperalgesia , biochemistry
Significance In this study, we identify microRNA-32-5p (miR-32-5p) as a key functional noncoding RNA in trigeminal-mediated neuropathic pain. We report that injury-induced histone methylation attenuates the binding of glucocorticoid receptor to the promoter region of themiR-32-5p gene and decreases the expression of miR-32-5p, in turn promoting the development of neuropathic pain through regulation of Cav3.2 channels. miRNA-mediated gene regulation has been proposed as a therapeutic approach in neuropathic pain. Our findings identify miR-32-5p replenishment as a therapeutic strategy for treating chronic neuropathic pain.