Evidence map›Paper›PMID 27435875›Full record

ArticleScientific reports2016

Glutathione peroxidase 3 localizes to the epithelial lining fluid and the extracellular matrix in interstitial lung disease.

Andrea C Schamberger, Herbert B Schiller, Isis E Fernandez, Martina Sterclova, Katharina Heinzelmann, Elisabeth Hennen, Rudolf Hatz, Jürgen Behr, Martina Vašáková, Matthias Mann and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 40 citations in OpenAlex.

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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

12 authors at 4 institutions in 2 countries.

Andrea C SchambergerComprehensive Pneumology Center, Helmholtz Zentrum München, Member of the German Center of Lung Research (DZL), Munich, Germany.
Herbert B SchillerComprehensive Pneumology Center, Helmholtz Zentrum München, Member of the German Center of Lung Research (DZL), Munich, Germany.
Isis E FernandezComprehensive Pneumology Center, Helmholtz Zentrum München, Member of the German Center of Lung Research (DZL), Munich, Germany.
Martina SterclovaDepartment of Respiratory Medicine of the 1st Medical School, Charles University and Thomayer Hospital, Prague, Czech republic.
Katharina HeinzelmannComprehensive Pneumology Center, Helmholtz Zentrum München, Member of the German Center of Lung Research (DZL), Munich, Germany.
Elisabeth HennenComprehensive Pneumology Center, Helmholtz Zentrum München, Member of the German Center of Lung Research (DZL), Munich, Germany.
Rudolf HatzThoraxchirurgisches Zentrum, Klinik für Allgemeine-, Viszeral-, Transplantations-, Gefäß- und Thoraxchirurgie, Klinikum Großhadern, Ludwig-Maximilians-Universität, Munich, Germany.
Jürgen BehrAsklepios Fachkliniken München-Gauting, Munich, Germany.
Martina VašákováDepartment of Respiratory Medicine of the 1st Medical School, Charles University and Thomayer Hospital, Prague, Czech republic.
Matthias MannDepartment of Proteomics and Signal Transduction, Max-Planck Institute of Biochemistry, Martinsried, Germany.
Oliver EickelbergComprehensive Pneumology Center, Helmholtz Zentrum München, Member of the German Center of Lung Research (DZL), Munich, Germany.
Claudia A Staab-WeijnitzComprehensive Pneumology Center, Helmholtz Zentrum München, Member of the German Center of Lung Research (DZL), Munich, Germany.
Helmholtz Zentrum München · DEAsklepios Fachkliniken München-Gauting · DECharles University · CZMax Planck Institute of Biochemistry · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant antioxidant activity and excessive deposition of extracellular matrix (ECM) are hallmarks of interstitial lung diseases (ILD). It is known that oxidative stress alters the ECM, but extracellular antioxidant defence mechanisms in ILD are incompletely understood. Here, we extracted abundance and detergent solubility of extracellular antioxidant enzymes from a proteomic dataset of bleomycin-induced lung fibrosis in mice and assessed regulation and distribution of glutathione peroxidase 3 (GPX3) in murine and human lung fibrosis. Superoxide dismutase 3 (Sod3), Gpx3, and Gpx activity were increased in mouse BALF during bleomycin-induced lung fibrosis. In lung tissue homogenates, Gpx3, but not Sod3, was upregulated and detergent solubility profiling indicated that Gpx3 associated with ECM proteins. Immunofluorescence analysis showed that Gpx3 was expressed by bronchial epithelial cells and interstitial fibroblasts and localized to the basement membrane and interstitial ECM in lung tissue. As to human ILD samples, BALF of some patients contained high levels of GPX3, and GPX3 was upregulated in lung homogenates from IPF patients. GPX3 expression in primary human bronchial epithelial cells and lung fibroblasts was downregulated by TNF-α, but more variably regulated by TGF-β1 and menadione. In conclusion, the antioxidant enzyme GPX3 localizes to lung ECM and is variably upregulated in ILD.

Indexed as

AgedAnimalsAntioxidantsBleomycinBronchiBronchoalveolar Lavage FluidDemographyDisease Models, AnimalDown-RegulationEpithelial CellsExtracellular MatrixFemaleFibroblastsGlutathione PeroxidaseHumansLung Diseases, InterstitialAntioxidantsBleomycinGlutathione PeroxidaseGPX3 protein, humanGpx3 protein, mouseTransforming Growth Factor beta1Tumor Necrosis Factor-alphaVitamin K 3

Identifiers

PMID27435875
PMCPMC4951690
OpenAlexW2498724094

What OpenQuestion holds

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LicenceCC BY
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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.