Evidence map›Paper›PMID 34429341›Full record

ArticleNeurology(R) neuroimmunology & neuroinflammation2021

Anti-contactin-1 Antibodies Affect Surface Expression and Sodium Currents in Dorsal Root Ganglia.

Julia Grüner, Helena Stengel, Christian Werner, Luise Appeltshauser, Claudia Sommer, Carmen Villmann, Kathrin Doppler

Open access · goldAbstract read
In one paragraph

Article in Neurology(R) neuroimmunology & neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
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  3. Article
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  5. Antibody-Mediated Nodo- and Paranodopathies.Journal of clinical medicine · 2024
    Review
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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

7 authors at 1 institution in 1 country.

Julia GrünerFrom the Department of Neurology (J.G., H.S., L.A., C.S., K.D.), University Hospital Würzburg, Germany; Department of Biotechnology and Biophysics (C.W.), Julius-Maximilians-University of Würzburg; and Institute of Clinical Neurobiology (C.V.), University Hospital, Julius-Maximilians-University of Würzburg, Germany.
Helena StengelFrom the Department of Neurology (J.G., H.S., L.A., C.S., K.D.), University Hospital Würzburg, Germany; Department of Biotechnology and Biophysics (C.W.), Julius-Maximilians-University of Würzburg; and Institute of Clinical Neurobiology (C.V.), University Hospital, Julius-Maximilians-University of Würzburg, Germany.
Christian WernerFrom the Department of Neurology (J.G., H.S., L.A., C.S., K.D.), University Hospital Würzburg, Germany; Department of Biotechnology and Biophysics (C.W.), Julius-Maximilians-University of Würzburg; and Institute of Clinical Neurobiology (C.V.), University Hospital, Julius-Maximilians-University of Würzburg, Germany.
Luise AppeltshauserFrom the Department of Neurology (J.G., H.S., L.A., C.S., K.D.), University Hospital Würzburg, Germany; Department of Biotechnology and Biophysics (C.W.), Julius-Maximilians-University of Würzburg; and Institute of Clinical Neurobiology (C.V.), University Hospital, Julius-Maximilians-University of Würzburg, Germany.ORCID 0000-0001-5248-4009
Claudia SommerFrom the Department of Neurology (J.G., H.S., L.A., C.S., K.D.), University Hospital Würzburg, Germany; Department of Biotechnology and Biophysics (C.W.), Julius-Maximilians-University of Würzburg; and Institute of Clinical Neurobiology (C.V.), University Hospital, Julius-Maximilians-University of Würzburg, Germany.
Carmen VillmannFrom the Department of Neurology (J.G., H.S., L.A., C.S., K.D.), University Hospital Würzburg, Germany; Department of Biotechnology and Biophysics (C.W.), Julius-Maximilians-University of Würzburg; and Institute of Clinical Neurobiology (C.V.), University Hospital, Julius-Maximilians-University of Würzburg, Germany.
Kathrin DopplerFrom the Department of Neurology (J.G., H.S., L.A., C.S., K.D.), University Hospital Würzburg, Germany; Department of Biotechnology and Biophysics (C.W.), Julius-Maximilians-University of Würzburg; and Institute of Clinical Neurobiology (C.V.), University Hospital, Julius-Maximilians-University of Würzburg, Germany. doppler_k@ukw.de.
University of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesAs autoantibodies to contactin-1 from patients with chronic inflammatory demyelinating polyradiculoneuropathy not only bind to the paranodes where they are supposed to cause conduction failure but also bind to other neuronal cell types, we aimed to investigate the effect of anti-contactin-1 autoantibodies on contactin-1 surface expression in cerebellar granule neurons, dorsal root ganglion neurons, and contactin-1-transfected human embryonic kidney 293 cells.

methodsImmunocytochemistry including structured illumination microscopy and immunoblotting was used to determine expression levels of contactin-1 and/or sodium channels after long-term exposure to autoantibodies from 3 seropositive patients. For functional analysis of sodium channels, whole-cell recordings of sodium currents were performed on dorsal root ganglion neurons incubated with anti-contactin-1 autoantibodies.

resultsWe found a reduction in contactin-1 expression levels on dorsal root ganglion neurons, cerebellar granule neurons, and contactin-1-transfected human embryonic kidney 293 cells and decreased dorsal root ganglion sodium currents after long-term exposure to anti-contactin-1 autoantibodies. Sodium channel density did not decrease. DISCUSSION: Our results demonstrate a direct effect of anti-contactin-1 autoantibodies on the surface expression of contactin-1 and sodium currents in dorsal root ganglion neurons. This may be the pathophysiologic correlate of sensory ataxia reported in these patients.

Indexed as

AutoantibodiesContactin 1Ganglia, SpinalHEK293 CellsHumansPolyneuropathiesSodiumSodium ChannelsAutoantibodiesContactin 1SodiumSodium Channels

Identifiers

PMID34429341
PMCPMC8407150
OpenAlexW3195491897

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.