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NaV1.6 and NaV1.7 channels are major endogenous voltage-gated sodium channels in ND7/23 cells

PloS one, 2019-08, Vol.14 (8), p.e0221156-e0221156 [Peer Reviewed Journal]

2019 Lee et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2019 Lee et al 2019 Lee et al ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0221156 ;PMID: 31419255

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Title:
NaV1.6 and NaV1.7 channels are major endogenous voltage-gated sodium channels in ND7/23 cells
Author: Lee, Jisoo ; Kim, Shinae ; Kim, Hye-Mi ; Kim, Hyun Jeong ; Yu, Frank H
Currie, Kevin P.M.
Subjects: Anesthesiology ; Animals ; Binding sites ; Biology and Life Sciences ; Cell adhesion & migration ; Cell Line, Tumor - drug effects ; Cell Line, Tumor - metabolism ; Deactivation ; Dental research ; Dentistry ; Electrophysiology ; Embryos ; Gene Expression Profiling ; Hybridomas - drug effects ; Hybridomas - metabolism ; Inactivation ; Ion Channel Gating - drug effects ; Ion channels ; Kinases ; Kinetics ; Medicine and Health Sciences ; Membrane Potentials - drug effects ; Mice ; Muscles ; Musculoskeletal system ; Mutation ; NAV1.6 Voltage-Gated Sodium Channel - metabolism ; NAV1.7 Voltage-Gated Sodium Channel - metabolism ; Neurobiology ; Neuroblastoma ; Neurons ; Neurosciences ; Pain ; Patch-Clamp Techniques ; Pharmacology ; Phosphorylation ; Physical Sciences ; Rats ; Research and Analysis Methods ; Reverse transcription ; Sensory neurons ; Skeletal muscle ; Sodium ; Sodium - metabolism ; Sodium Channel Blockers - pharmacology ; Sodium channels (voltage-gated) ; Tetrodotoxin ; Tetrodotoxin - pharmacology
Is Part Of: PloS one, 2019-08, Vol.14 (8), p.e0221156-e0221156
Description: ND7/23 cells are gaining traction as a host model to express peripheral sodium channels such as NaV1.8 and NaV1.9 that have been difficult to express in widely utilized heterologous cells, like CHO and HEK293. Use of ND7/23 as a model cell to characterize the properties of sodium channels requires clear understanding of the endogenous ion channels. To define the nature of the background sodium currents in ND7/23 cells, we aimed to comprehensively profile the voltage-gated sodium channel subunits by endpoint and quantitative reverse transcription-PCR and by whole-cell patch clamp electrophysiology. We found that untransfected ND7/23 cells express endogenous peak sodium currents that average -2.12nA (n = 15) and with kinetics typical of fast sodium currents having activation and inactivation completed within few milliseconds. Furthermore, sodium currents were reduced to virtually nil upon exposure to 100nM tetrodotoxin, indicating that ND7/23 cells have essentially null background for tetrodotoxin-resistant (TTX-R) currents. qRT-PCR profiling indicated a major expression of TTX-sensitive (TTX-S) NaV1.6 and NaV1.7 at similar levels and very low expression of TTX-R NaV1.9 transcripts. There was no expression of TTX-R NaV1.8 in ND7/23 cells. There was low expression of NaV1.1, NaV1.2, NaV1.3 and no expression of cardiac or skeletal muscle sodium channels. As for the sodium channel auxiliary subunits, β1 and β3 subunits were expressed, but not the β2 and β4 subunits that covalently associate with the α-subunits. In addition, our results also showed that only the mouse forms of NaV1.6, NaV1.7 and NaV1.9 sodium channels were expressed in ND7/23 cells that was originally generated as a hybridoma of rat embryonic DRG and mouse neuroblastoma cell-line. By molecular profiling of auxiliary β- and principal α-subunits of the voltage gated sodium channel complex, our results define the background sodium channels expressed in ND7/23 cells, and confirm their utility for detailed functional studies of emerging pain channelopathies ascribed to mutations of the TTX-R sodium channels of sensory neurons.
Publisher: United States: Public Library of Science
Language: English
Identifier: ISSN: 1932-6203
EISSN: 1932-6203
DOI: 10.1371/journal.pone.0221156
PMID: 31419255
Source: Geneva Foundation Free Medical Journals at publisher websites
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NaV1.6 and NaV1.7 channels are major endogenous voltage-gated sodium channels in ND7/23 cells

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