Evidence map›Paper›PMID 39982575›Full record

ArticleJournal of molecular neuroscience : MN2025

SOX10-Mediated Regulation of Enteric Glial Phenotype in vitro and its Relevance for Neuroinflammatory Disorders.

Madlen Kunke, Meike Kaehler, Sebastien Boni, Katja Schröder, Alicia Weier, Rittika Chunder, Stefanie Kuerten, Martina Böttner, Ingolf Cascorbi, Michel Neunlist and 3 more

Abstract read
In one paragraph

Article in Journal of molecular neuroscience : MN, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
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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

13 authors.

Madlen KunkeInstitute of Anatomy, Kiel University, Kiel, Germany.
Meike KaehlerInstitute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Sebastien BoniLentivec Platform, Université d'Angers, Angers, France.
Katja SchröderInstitute of Anatomy, Kiel University, Kiel, Germany.
Alicia WeierInstitute of Neuroanatomy, Medical Faculty, University of Bonn and University Hospital Bonn, Bonn, Germany.
Rittika ChunderInstitute of Neuroanatomy, Medical Faculty, University of Bonn and University Hospital Bonn, Bonn, Germany.
Stefanie KuertenInstitute of Neuroanatomy, Medical Faculty, University of Bonn and University Hospital Bonn, Bonn, Germany.
Martina BöttnerInstitute of Anatomy, Kiel University, Kiel, Germany.
Ingolf CascorbiInstitute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Michel NeunlistNantes University, Inserm, TENS, the Enteric Nervous System in Gut and Brain Diseases, IMAD, Nantes, France.
Thilo WedelInstitute of Anatomy, Kiel University, Kiel, Germany.
Ralph LuciusInstitute of Anatomy, Kiel University, Kiel, Germany.
François CossaisInstitute of Anatomy, Kiel University, Kiel, Germany. f.cossais@anat.uni-kiel.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor SOX10 is a key regulator of myelinated glial cell phenotype and function, with a known role in multiple sclerosis (MS). SOX10 is also expressed in enteric glial cells (EGC) within the gut, yet its regulatory functions in EGC remain poorly understood. This study aimed to identify SOX10 target genes that influence EGC phenotype and may have implications for MS. An EGC cell line was established for doxycycline-inducible SOX10 overexpression. Impact of SOX10 overexpression on EGC phenotype was assessed by genome-wide expression analysis and results were validated via RT-qPCR and western blot. Data were compared with SOX10 ChIP-seq and transcriptomic datasets from MS patients to identify pan-glial SOX10 target genes potentially linked to neuroinflammatory disorders. SOX10 overexpression was associated with ectopic upregulation of genes related to myelin regulation and glial differentiation, as evidenced by increased PLP1 expression at mRNA and protein levels. Comparison to ChIP-seq and MS datasets highlight SOX10 target genes, including PLP1, RNF130, NES and APOD potentially involved in central and peripheral manifestations of MS pathology. Our findings support a cell-specific regulation of EGC phenotype through SOX10 expression level and identify SOX10-regulated genes relevant to EGC function. This research advances the understanding of EGC diversity and provide information about glial cells targeting in neuroinflammatory disorders.

Indexed as

Enteric Nervous SystemNeurogliaNeuroinflammatory DiseasesSOXE Transcription FactorsCell LineHumansMultiple SclerosisPhenotypeSOX10 protein, humanSOXE Transcription FactorsEnteric glial cellsMultiple sclerosisNestinNeuroinflammationPLP1Schwann cellSox10

Identifiers

PMID39982575
PMCPMC11845537

What OpenQuestion holds

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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.