Evidence map›Paper›PMID 40380298›Full record

ArticleCell communication and signaling : CCS2025

Repression of Connexin26 hemichannel activity protects the barrier function of respiratory airway epithelial cells against LPS-induced alteration.

Tina Lehrich, Anne Dierks, Masina Plenge, Helena Obernolte, Klaudia Grieger, Katherina Sewald, Frederic Rodriguez, Lucie Malet, Peter Braubach, Florence Bedos-Belval and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Tina Lehrich *Institute of Cell Biology and Biophysics, Department of Cell Physiology and Biophysics, Leibniz University Hannover, Hannover, Germany.ORCID http://orcid.org/0000-0002-3450-1300
Anne Dierks *Institute of Cell Biology and Biophysics, Department of Cell Physiology and Biophysics, Leibniz University Hannover, Hannover, Germany.ORCID http://orcid.org/0000-0001-5382-3631
Masina PlengeInstitute of Cell Biology and Biophysics, Department of Cell Physiology and Biophysics, Leibniz University Hannover, Hannover, Germany.ORCID http://orcid.org/0000-0002-4202-0283
Helena ObernolteFraunhofer Institute for Toxicology and Experimental Medicine (ITEM), Division of Preclinical Pharmacology and Toxicology, Hannover, Germany.ORCID http://orcid.org/0000-0002-3634-066X
Klaudia GriegerFraunhofer Institute for Toxicology and Experimental Medicine (ITEM), Division of Preclinical Pharmacology and Toxicology, Hannover, Germany.ORCID http://orcid.org/0009-0005-7181-3150
Katherina SewaldFraunhofer Institute for Toxicology and Experimental Medicine (ITEM), Division of Preclinical Pharmacology and Toxicology, Hannover, Germany.ORCID http://orcid.org/0000-0001-7137-4171
Frederic RodriguezLaboratoire de Synthèse et Physicochimie des Molécules d'Intérêt Biologique, CNRS, UMR 5068, Toulouse, France.ORCID http://orcid.org/0000-0001-9192-6973
Lucie MaletLaboratoire de Synthèse et Physicochimie des Molécules d'Intérêt Biologique, CNRS, UMR 5068, Toulouse, France.ORCID http://orcid.org/0009-0000-5871-1532
Peter BraubachBiomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), German Centre for Lung Research, Hannover Medical School, Hannover, Germany.ORCID http://orcid.org/0000-0003-3673-7779
Florence Bedos-BelvalLaboratoire de Synthèse et Physicochimie des Molécules d'Intérêt Biologique, CNRS, UMR 5068, Toulouse, France.ORCID http://orcid.org/0000-0002-6792-6815
Anaclet NgezahayoInstitute of Cell Biology and Biophysics, Department of Cell Physiology and Biophysics, Leibniz University Hannover, Hannover, Germany. ngezahayo@cell.uni-hannover.de.ORCID http://orcid.org/0000-0002-3686-923X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In respiratory airway epithelial cells, lipopolysaccharide (LPS) treatment induced an enhancement of connexin 26 (Cx26) hemichannel activity shown by dye uptake experiments after siRNA-mediated knock-down of Cx26. This effect was already observed at infection relevant concentrations (≤ 10 ng/mL LPS) and involved tumor necrosis factor alpha (TNF-α)- and Ca

Indexed as

Connexin 26ConnexinsEpithelial CellsLipopolysaccharidesRespiratory MucosaCell LineClaudin-4HumansMolecular Docking SimulationTight JunctionsTumor Necrosis Factor-alphaClaudin-4Connexin 26ConnexinsLipopolysaccharidesTumor Necrosis Factor-alphaAirway epitheliumBarrier functionCalu-3 cellsConnexin channels; lipopolysaccharideCytokinePCLSPrimary cells

Identifiers

PMID40380298
PMCPMC12082868

What OpenQuestion holds

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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.