Evidence map›Paper›PMID 26321143›Full record

ArticleStem cell reports2015

Pattern of Functional TTX-Resistant Sodium Channels Reveals a Developmental Stage of Human iPSC- and ESC-Derived Nociceptors.

Esther Eberhardt, Steven Havlicek, Diana Schmidt, Andrea S Link, Cristian Neacsu, Zacharias Kohl, Martin Hampl, Andreas M Kist, Alexandra Klinger, Carla Nau and 6 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.4field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
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  8. Calcium-sensing receptor regulates Kv7 channels via GBritish journal of pharmacology · 2024
    Article
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  19. iPSCs and DRGs: stepping stones to new pain therapies.Trends in molecular medicine · 2022
    Review
  20. Differentiation of iPS-Cells into Peripheral Sensory Neurons.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 1 country.

Esther EberhardtInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsstraße 17, 91054 Erlangen, Germany; Department of Anesthesiology, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Krankenhausstrasse 12, 91054 Erlangen, Germany.
Steven HavlicekIZKF Junior Research Group and BMBF Research Group Neuroscience, IZKF, Friedrich-Alexander-Universität Erlangen-Nürnberg, Glückstrasse 6, 91054 Erlangen, Germany.
Diana SchmidtInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsstraße 17, 91054 Erlangen, Germany; IZKF Junior Research Group and BMBF Research Group Neuroscience, IZKF, Friedrich-Alexander-Universität Erlangen-Nürnberg, Glückstrasse 6, 91054 Erlangen, Germany.
Andrea S LinkInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsstraße 17, 91054 Erlangen, Germany.
Cristian NeacsuInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsstraße 17, 91054 Erlangen, Germany.
Zacharias KohlDepartment of Molecular Neurology, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Schwabachanlage 6, 91054 Erlangen, Germany.
Martin HamplInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsstraße 17, 91054 Erlangen, Germany; Institute of Physiology, Uniklinik RWTH Aachen, Pauwelsstrasse 30, 52074 Aachen, Germany.
Andreas M KistInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsstraße 17, 91054 Erlangen, Germany.
Alexandra KlingerInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsstraße 17, 91054 Erlangen, Germany.
Carla NauDepartment of Anesthesiology and Intensive Care, University Medical Center Schleswig-Holstein, Campus Luebeck, Ratzeburger Allee 160, 23538 Lübeck, Germany.
Jürgen SchüttlerDepartment of Anesthesiology, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Krankenhausstrasse 12, 91054 Erlangen, Germany.
Christian AlzheimerInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsstraße 17, 91054 Erlangen, Germany.
Jürgen WinklerDepartment of Molecular Neurology, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Schwabachanlage 6, 91054 Erlangen, Germany.
Barbara NamerInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsstraße 17, 91054 Erlangen, Germany.
Beate WinnerIZKF Junior Research Group and BMBF Research Group Neuroscience, IZKF, Friedrich-Alexander-Universität Erlangen-Nürnberg, Glückstrasse 6, 91054 Erlangen, Germany. Electronic address: beate.winner@med.uni-erlangen.de.
Angelika LampertInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsstraße 17, 91054 Erlangen, Germany; Institute of Physiology, Uniklinik RWTH Aachen, Pauwelsstrasse 30, 52074 Aachen, Germany. Electronic address: alampert@ukaachen.de.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversitätsklinikum Aachen · DEUniversitätsklinikum Erlangen · DEUniversity Hospital Schleswig-Holstein · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human pluripotent stem cells (hPSCs) offer the opportunity to generate neuronal cells, including nociceptors. Using a chemical-based approach, we generated nociceptive sensory neurons from HUES6 embryonic stem cells and retrovirally reprogrammed induced hPSCs derived from fibroblasts. The nociceptive neurons expressed respective markers and showed tetrodotoxin-sensitive (TTXs) and -resistant (TTXr) voltage-gated sodium currents in patch-clamp experiments. In contrast to their counterparts from rodent dorsal root ganglia, TTXr currents of hPSC-derived nociceptors unexpectedly displayed a significantly more hyperpolarized voltage dependence of activation and fast inactivation. This apparent discrepancy is most likely due to a substantial expression of the developmentally important sodium channel NAV1.5. In view of the obstacles to recapitulate neuropathic pain in animal models, our data advance hPSC-derived nociceptors as a better model to study developmental and pathogenetic processes in human nociceptive neurons and to develop more specific small molecules to attenuate pain.

Indexed as

Cell DifferentiationAnimalsCell LineGanglia, SpinalHuman Embryonic Stem CellsHumansInduced Pluripotent Stem CellsIon Channel GatingNAV1.5 Voltage-Gated Sodium ChannelNociceptorsRatsTetrodotoxinNAV1.5 Voltage-Gated Sodium ChannelSCN5A protein, humanTetrodotoxin

Identifiers

PMID26321143
PMCPMC4618592
OpenAlexW1924826612

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.