Evidence map›Paper›PMID 29472603›Full record

ArticleScientific reports2018

Bronchial extracellular matrix from COPD patients induces altered gene expression in repopulated primary human bronchial epithelial cells.

Ulf Hedström, Oskar Hallgren, Lisa Öberg, Amy DeMicco, Outi Vaarala, Gunilla Westergren-Thorsson, Xiaohong Zhou

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Study on the changes of extracellular matrix morphology and components in COPD animal model by using lung decellularized scaffold.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Chronic lung diseases: prospects for regeneration and repair.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
  13. Why new biology must be uncovered to advance therapeutic strategies for chronic obstructive pulmonary disease.American journal of physiology. Lung cellular and molecular physiology · 2021
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Acellular human lung scaffolds to model lung disease and tissue regeneration.European respiratory review : an official journal of the European Respiratory Society · 2018
    Review
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 3 institutions in 2 countries.

Ulf HedströmBioscience Regeneration Department, Respiratory, Inflammation and Autoimmunity, IMED Biotech Unit, AstraZeneca, Gothenburg, Sweden.
Oskar HallgrenDivision of Lung Biology, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Lisa ÖbergBioscience Immunity Department, Respiratory, Inflammation and Autoimmunity, IMED Biotech Unit, AstraZeneca, Gothenburg, Sweden.ORCID 0000-0001-7127-1711
Amy DeMiccoBioscience Regeneration Department, Respiratory, Inflammation and Autoimmunity, IMED Biotech Unit, AstraZeneca, Gothenburg, Sweden.
Outi VaaralaBioscience Immunity Department, Respiratory, Inflammation and Autoimmunity, IMED Biotech Unit, AstraZeneca, Gothenburg, Sweden.
Gunilla Westergren-ThorssonDivision of Lung Biology, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Xiaohong ZhouBioscience Regeneration Department, Respiratory, Inflammation and Autoimmunity, IMED Biotech Unit, AstraZeneca, Gothenburg, Sweden. Xiao-Hong.Zhou@astrazeneca.com.
AstraZeneca (Sweden) · SELund University · SEAstraZeneca (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a serious global health problem characterized by chronic airway inflammation, progressive airflow limitation and destruction of lung parenchyma. Remodeling of the bronchial airways in COPD includes changes in both the bronchial epithelium and the subepithelial extracellular matrix (ECM). To explore the impact of an aberrant ECM on epithelial cell phenotype in COPD we developed a new ex vivo model, in which normal human bronchial epithelial (NHBE) cells repopulate and differentiate on decellularized human bronchial scaffolds derived from COPD patients and healthy individuals. By using transcriptomics, we show that bronchial ECM from COPD patients induces differential gene expression in primary NHBE cells when compared to normal bronchial ECM. The gene expression profile indicated altered activity of upstream mediators associated with COPD pathophysiology, including hepatocyte growth factor, transforming growth factor beta 1 and platelet-derived growth factor B, which suggests that COPD-related changes in the bronchial ECM contribute to the defective regenerative ability in the airways of COPD patients.

Indexed as

BronchiConnective Tissue Growth FactorEpithelial CellsExtracellular MatrixGene Expression RegulationHepatocyte Growth FactorHumansLungPrimary Cell CultureProto-Oncogene Proteins c-sisPulmonary Disease, Chronic ObstructiveRespiratory MucosaTranscriptomeTransforming Growth Factor beta1CCN2 protein, humanConnective Tissue Growth FactorHepatocyte Growth FactorHGF protein, humanProto-Oncogene Proteins c-sisTransforming Growth Factor beta1

Identifiers

PMID29472603
PMCPMC5823945
OpenAlexW2794536406

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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.