2. Academic Validation
  3. Nuclear Factor-kappaB Gates Nav1.7 Channels in DRG Neurons via Protein-Protein Interaction

Nuclear Factor-kappaB Gates Nav1.7 Channels in DRG Neurons via Protein-Protein Interaction

  • iScience. 2019 Sep 27;19:623-633. doi: 10.1016/j.isci.2019.08.017.
Man-Xiu Xie 1,  Xiao-Long Zhang 2,  Jing Xu 3,  Wei-An Zeng 1,  Dai Li 3,  Ting Xu 3,  Rui-Ping Pang 3,  Ke Ma 4,  Xian-Guo Liu 5
Affiliations

Affiliations

  • 1 Department of Anesthesiology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, 651 Dongfeng East Road, Guangzhou 510060, China.
  • 2 Medical Research Center of Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, 106 Zhongshan Road 2, Guangzhou 510080, China.
  • 3 Pain Research Center and Department of Physiology, Zhongshan School of Medicine of Sun Yat-sen University, 74 Zhongshan Road 2, Guangzhou 510080, China.
  • 4 Department of Pain Management, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 91603, China. Electronic address: [email protected].
  • 5 Pain Research Center and Department of Physiology, Zhongshan School of Medicine of Sun Yat-sen University, 74 Zhongshan Road 2, Guangzhou 510080, China; Department of Pain Management, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 91603, China; Guangdong Provincial Key Laboratory of Brain Function and Disease, 74 Zhongshan Road 2, Guangzhou 510080, China. Electronic address: [email protected].
PMID: 31446225 DOI: 10.1016/j.isci.2019.08.017
Abstract

It is well known that nuclear factor-kappaB (NF-κB) regulates neuronal structures and functions by nuclear transcription. Here, we showed that phospho-p65 (p-p65), an active form of NF-κB subunit, reversibly interacted with Nav1.7 channels in the membrane of dorsal root ganglion (DRG) neurons of rats. The interaction increased Nav1.7 currents by slowing inactivation of Nav1.7 channels and facilitating their recovery from inactivation, which may increase the resting state of the channels ready for activation. In cultured DRG neurons TNF-α upregulated the membrane p-p65 and enhanced Nav1.7 currents within 5 min but did not affect nuclear NF-κB within 40 min. This non-transcriptional effect on Nav1.7 may underlie a rapid regulation of the sensibility of the somatosensory system. Both NF-κB and Nav1.7 channels are critically implicated in many physiological functions and diseases. Our finding may shed new LIGHT on the investigation into the underlying mechanisms.

Keywords

Biological Sciences; Cellular Neuroscience; Molecular Neuroscience; Neuroscience.

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