ArticleInternational journal of molecular medicine2020
Upregulation of Nav1.7 by endogenous hydrogen sulfide contributes to maintenance of neuropathic pain.
Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- The Role of Hydrogen Sulfide in Peripheral Nervous System Modulation.Handbook of experimental pharmacology · 2026Review
- Benzydamine-An Affordable Over-the-Counter Drug with Psychoactive Properties-From Chemical Structure to Possible Pharmacological Properties.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Plant and fungi derived analgesic natural products targeting voltage-gated sodium and calcium channels.Channels (Austin, Tex.) · 2022Review
- Analgesia effect of lentivirus-siSCN9A infected neurons in vincristine induced neuropathic pain rats.Bioengineered · 2021Article
- Review
- Improving NKCC1 Function Increases the Excitability of DRG Neurons Exacerbating Pain Induced After TRPV1 Activation of Primary Sensory Neurons.Frontiers in cellular neuroscience · 2021Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
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Abstract
Nav1.7 is closely associated with neuropathic pain. Hydrogen sulfide (H2S) has recently been reported to be involved in numerous biological functions, and it has been shown that H2S can enhance the sodium current density, and inhibiting the endogenous production of H2S mediated by cystathionine β‑synthetase (CBS) using O‑(carboxymethyl)hydroxylamine hemihydrochloride (AOAA) can significantly reduce the expression of Nav1.7 and thus the sodium current density in rat dorsal root ganglion (DRG) neurons. In the present study, it was shown that the fluorescence intensity of H2S was increased in a spared nerve injury (SNI) model and AOAA inhibited this increase. Nav1.7 is expressed in DRG neurons, and the expression of CBS and Nav1.7 were increased in DRG neurons 7, 14 and 21 days post‑operation. AOAA inhibited the increase in the expression of CBS, phosphorylated (p)‑MEK1/2, p‑ERK1/2 and Nav1.7 induced by SNI, and U0126 (a MEK blocker) was able to inhibit the increase in p‑MEK1/2, p‑ERK1/2 and Nav1.7 expression. However, PF‑04856264 did not inhibit the increase in CBS, p‑MEK1/2, p‑ERK1/2 or Nav1.7 expression induced by SNI surgery. The current density of Nav1.7 was significantly increased in the SNI model and administration of AOAA and U0126 both significantly decreased the density. In addition, AOAA, U0126 and PF‑04856264 inhibited the decrease in rheobase, and the increase in action potential induced by SNI in DRG neurons. There was no significant difference in thermal withdrawal latency among each group. However, the time the animals spent with their paw lifted increased significantly following SNI, and the time the animals spent with their paw lifted decreased significantly following the administration of AOAA, U0126 and PF‑04856264. In conclusion, these data show that Nav1.7 expression in DRG neurons is upregulated by CBS‑derived endogenous H2S in an SNI model, contributing to the maintenance of neuropathic pain.
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