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NGF-Induced Nav1.7 Upregulation Contributes to Chronic Post-surgical Pain by Activating SGK1-Dependent Nedd4-2
Bao-Wen Liu1, Jin Zhang1, Yi-Shun Hong1
1Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Molecular Neurobiology
|October 16, 2020
Summary
Nerve growth factor (NGF) may cause long-term dysregulation of the Nav1.7 sodium channel, contributing to chronic post-surgical pain (CPSP). Targeting Nav1.7 in peripheral nociceptors could prevent CPSP development.
Area of Science:
- Neuroscience
- Pain Research
- Molecular Biology
Background:
- Chronic post-surgical pain (CPSP) mechanisms remain poorly understood, hindering effective prevention and treatment.
- Surgical injury upregulates voltage-gated sodium channel Nav1.7 in dorsal root ganglion (DRG) neurons, implicating it in CPSP.
- Nerve growth factor (NGF) is known to induce long-term neuronal hyperexcitability after injury.
Purpose of the Study:
- To investigate if NGF-mediated regulation of Nav1.7 contributes to CPSP.
- To elucidate the specific mechanisms underlying NGF's role in CPSP development.
- To explore potential therapeutic strategies targeting the NGF-Nav1.7 pathway.
Main Methods:
- Utilized conditional nociceptor-specific Nav1.7 knockout mice for pain behavior analysis.
- Employed western blot and immunostaining to assess Nav1.7 expression changes in rats.
- Applied pharmacological approaches to investigate the NGF/TrkA-SGK1-Nedd4-2 pathway.
- Evaluated the effect of reversing Nav1.7 upregulation on spinal sensitization.
Main Results:
- Confirmed Nav1.7 involvement in NGF-induced pain and its role in maintaining pain behavior for up to 14 days.
- Demonstrated that NGF triggers Nav1.7 upregulation, supporting CPSP development in rats.
- Identified a potential regulatory pathway: NGF/TrkA-SGK1-Nedd4-2 mediating Nav1.7 increase.
- Showed that reversing Nav1.7 upregulation in DRG alleviates spinal sensitization.
Conclusions:
- Maintained Nav1.7 upregulation, induced by NGF, significantly contributes to CPSP development.
- Targeting Nav1.7 dysregulation in peripheral nociceptors presents a potential strategy to prevent acute-to-chronic pain transition.
- Understanding the NGF-Nav1.7 interaction offers new avenues for CPSP therapeutic interventions.
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