Nuclear Factor-kappaB Gates Nav1.7 Channels in DRG Neurons via Protein-Protein Interaction
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 rat...
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| Published in | iScience Vol. 19; pp. 623 - 633 |
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| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
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27.09.2019
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| 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.
[Display omitted]
•NF-κB p-p65 interacts with Nav1.7 in the membrane of DRG neurons•The interaction is reversible, depending on the cytoplasmic p-p65 content•Reducing cytoplasmic p-p65 rapidly attenuates the interaction and Nav1.7 currents•The rapid effect on Nav1.7 channels is independent of p-p65 nuclear translocation
Biological Sciences; Neuroscience; Molecular Neuroscience; Cellular Neuroscience |
|---|---|
| AbstractList | 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 Na
v
1.7 channels in the membrane of dorsal root ganglion (DRG) neurons of rats. The interaction increased Na
v
1.7 currents by slowing inactivation of Na
v
1.7 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 Na
v
1.7 currents within 5 min but did not affect nuclear NF-κB within 40 min. This non-transcriptional effect on Na
v
1.7 may underlie a rapid regulation of the sensibility of the somatosensory system. Both NF-κB and Na
v
1.7 channels are critically implicated in many physiological functions and diseases. Our finding may shed new light on the investigation into the underlying mechanisms.
•
NF-κB
p
-p65 interacts with Na
v
1.7 in the membrane of DRG neurons
•
The interaction is reversible, depending on the cytoplasmic
p
-p65 content
•
Reducing cytoplasmic
p
-p65 rapidly attenuates the interaction and Na
v
1.7 currents
•
The rapid effect on Na
v
1.7 channels is independent of
p
-p65 nuclear translocation
Biological Sciences; Neuroscience; Molecular Neuroscience; Cellular Neuroscience 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. [Display omitted] •NF-κB p-p65 interacts with Nav1.7 in the membrane of DRG neurons•The interaction is reversible, depending on the cytoplasmic p-p65 content•Reducing cytoplasmic p-p65 rapidly attenuates the interaction and Nav1.7 currents•The rapid effect on Nav1.7 channels is independent of p-p65 nuclear translocation Biological Sciences; Neuroscience; Molecular Neuroscience; Cellular Neuroscience 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.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. 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. : Biological Sciences; Neuroscience; Molecular Neuroscience; Cellular Neuroscience Subject Areas: Biological Sciences, Neuroscience, Molecular Neuroscience, Cellular Neuroscience |
| Author | Zeng, Wei-An Xu, Jing Ma, Ke Xie, Man-Xiu Zhang, Xiao-Long Pang, Rui-Ping Li, Dai Liu, Xian-Guo Xu, Ting |
| AuthorAffiliation | 5 Medical Research Center of Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, 106 Zhongshan Road 2, Guangzhou 510080, China 3 Department of Pain Management, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 91603, China 4 Guangdong Provincial Key Laboratory of Brain Function and Disease, 74 Zhongshan Road 2, Guangzhou 510080, China 2 Pain Research Center and Department of Physiology, Zhongshan School of Medicine of Sun Yat-sen University, 74 Zhongshan Road 2, Guangzhou 510080, China 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 |
| AuthorAffiliation_xml | – name: 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 – name: 3 Department of Pain Management, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 91603, China – name: 4 Guangdong Provincial Key Laboratory of Brain Function and Disease, 74 Zhongshan Road 2, Guangzhou 510080, China – name: 5 Medical Research Center of Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, 106 Zhongshan Road 2, Guangzhou 510080, China – name: 2 Pain Research Center and Department of Physiology, Zhongshan School of Medicine of Sun Yat-sen University, 74 Zhongshan Road 2, Guangzhou 510080, China |
| Author_xml | – sequence: 1 givenname: Man-Xiu surname: Xie fullname: Xie, Man-Xiu organization: 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 – sequence: 2 givenname: Xiao-Long surname: Zhang fullname: Zhang, Xiao-Long organization: Medical Research Center of Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, 106 Zhongshan Road 2, Guangzhou 510080, China – sequence: 3 givenname: Jing surname: Xu fullname: Xu, Jing organization: Pain Research Center and Department of Physiology, Zhongshan School of Medicine of Sun Yat-sen University, 74 Zhongshan Road 2, Guangzhou 510080, China – sequence: 4 givenname: Wei-An surname: Zeng fullname: Zeng, Wei-An organization: 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 – sequence: 5 givenname: Dai surname: Li fullname: Li, Dai organization: Pain Research Center and Department of Physiology, Zhongshan School of Medicine of Sun Yat-sen University, 74 Zhongshan Road 2, Guangzhou 510080, China – sequence: 6 givenname: Ting surname: Xu fullname: Xu, Ting organization: Pain Research Center and Department of Physiology, Zhongshan School of Medicine of Sun Yat-sen University, 74 Zhongshan Road 2, Guangzhou 510080, China – sequence: 7 givenname: Rui-Ping surname: Pang fullname: Pang, Rui-Ping organization: Pain Research Center and Department of Physiology, Zhongshan School of Medicine of Sun Yat-sen University, 74 Zhongshan Road 2, Guangzhou 510080, China – sequence: 8 givenname: Ke surname: Ma fullname: Ma, Ke email: marke72@163.com organization: Department of Pain Management, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 91603, China – sequence: 9 givenname: Xian-Guo orcidid: 0000-0002-4352-8687 surname: Liu fullname: Liu, Xian-Guo email: liuxg@mail.sysu.edu.cn organization: Pain Research Center and Department of Physiology, Zhongshan School of Medicine of Sun Yat-sen University, 74 Zhongshan Road 2, Guangzhou 510080, China |
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| Snippet | It is well known that nuclear factor-kappaB (NF-κB) regulates neuronal structures and functions by nuclear transcription. Here, we showed that phospho-p65... 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... |
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| Title | Nuclear Factor-kappaB Gates Nav1.7 Channels in DRG Neurons via Protein-Protein Interaction |
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