Evidence map›Paper›PMID 39578767›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

Co-culture of human AT2 cells with fibroblasts reveals a MUC5B phenotype: insights from an organoid model.

Yiwen Yao, Felix Ritzmann, Sarah Miethe, Kathrin Kattler-Lackes, Betül Colakoglu, Christian Herr, Andreas Kamyschnikow, Michelle Brand, Holger Garn, Daniela Yildiz and 3 more

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. 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
–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

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

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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.

Yiwen YaoDepartment of Internal Medicine V - Pulmonology, Allergology and Critical Care Medicine, Saarland University, 66421, Homburg, Germany.
Felix RitzmannDepartment of Internal Medicine V - Pulmonology, Allergology and Critical Care Medicine, Saarland University, 66421, Homburg, Germany.
Sarah MietheTranslational Inflammation Research Division & Core Facility for Single Cell Multiomics, Medical Faculty, Member of the German Center for Lung Research (DZL) and the Universities of Giessen and Marburg Lung Center, Philipps University of Marburg, D-35043, Marburg, Germany.
Kathrin Kattler-LackesDepartment of Genetics/Epigenetics, Saarland University, 66123, Saarbrücken, Germany.
Betül ColakogluDepartment of Internal Medicine V - Pulmonology, Allergology and Critical Care Medicine, Saarland University, 66421, Homburg, Germany.
Christian HerrDepartment of Internal Medicine V - Pulmonology, Allergology and Critical Care Medicine, Saarland University, 66421, Homburg, Germany.
Andreas KamyschnikowDepartment of Internal Medicine V - Pulmonology, Allergology and Critical Care Medicine, Saarland University, 66421, Homburg, Germany.
Michelle BrandDepartment of Internal Medicine V - Pulmonology, Allergology and Critical Care Medicine, Saarland University, 66421, Homburg, Germany.
Holger GarnTranslational Inflammation Research Division & Core Facility for Single Cell Multiomics, Medical Faculty, Member of the German Center for Lung Research (DZL) and the Universities of Giessen and Marburg Lung Center, Philipps University of Marburg, D-35043, Marburg, Germany.
Daniela YildizExperimental and Clinical Pharmacology and Toxicology, PZMS, Saarland University, 66421, Homburg, Germany.
Frank LangerDepartment of Thoracic- and Cardiovascular Surgery, Saarland University Hospital, Homburg/Saar, Germany.
Robert BalsDepartment of Internal Medicine V - Pulmonology, Allergology and Critical Care Medicine, Saarland University, 66421, Homburg, Germany.
Christoph BeisswengerDepartment of Internal Medicine V - Pulmonology, Allergology and Critical Care Medicine, Saarland University, 66421, Homburg, Germany. christoph.beisswenger@uks.eu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Impaired interaction of fibroblasts with pneumocytes contributes to the progression of chronic lung disease such as idiopathic pulmonary fibrosis (IPF). Mucin 5B (MUC5B) is associated with IPF. Here we analyzed the interaction of primary fibroblasts and alveolar type 2 (AT2) pneumocytes in the organoid model. Single-cell analysis, histology, and qRT-PCR revealed that fibroblasts expressing high levels of fibrosis markers regulate STAT3 signaling in AT2 cells, which is accompanied by cystic organoid growth and MUC5B expression. Cystic growth and MUC5B expression were also caused by the cytokine IL-6. The PI3K-Akt signaling pathway was activated in fibroblasts. The drug dasatinib prevented the formation of MUC5B-expressing cystic organoids. MUC5B associated with AT2 cells in samples obtained from IPF patients. Our model shows that fibrotic primary fibroblasts induce impaired differentiation of AT2 cells via STAT3 signaling pathways, as observed in IPF patients. It can be used for mechanistic studies and drug development.

Indexed as

Alveolar Epithelial CellsCoculture TechniquesFibroblastsIdiopathic Pulmonary FibrosisMucin-5BOrganoidsSignal TransductionSTAT3 Transcription FactorCell DifferentiationHumansInterleukin-6PhenotypeInterleukin-6MUC5B protein, humanMucin-5BSTAT3 protein, humanSTAT3 Transcription FactorFibroblastIPFOrganoidPneumocyteSTAT3

Identifiers

PMID39578767
PMCPMC11585087

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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.