Evidence map›Paper›PMID 20459817›Full record

ArticleRespiratory research2010

Altered fibroblast proteoglycan production in COPD.

Oskar Hallgren, Kristian Nihlberg, Magnus Dahlbäck, Leif Bjermer, Leif T Eriksson, Jonas S Erjefält, Claes-Göran Löfdahl, Gunilla Westergren-Thorsson

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In one paragraph

Article in Respiratory research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

63 citing papers in PubMed, 106 citations in OpenAlex.

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  10. Small airway fibroblasts from patients with chronic obstructive pulmonary disease exhibit cellular senescence.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  11. Article
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  13. Frontiers in bioengineering and biotechnology · 2023
    Review
  14. From COPD to Lung Cancer: Mechanisms Linking, Diagnosis, Treatment, and Prognosis.International journal of chronic obstructive pulmonary disease · 2022
    Review
  15. Review
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3 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Oskar HallgrenDepartment of Experimental Medical Science, BMC D12 Lund, Lund University, Sweden. oskar.hallgren@med.lu.se
Kristian Nihlberg
Magnus Dahlbäck
Leif Bjermer
Leif T Eriksson
Jonas S Erjefält
Claes-Göran Löfdahl
Gunilla Westergren-Thorsson
Lund University · SEAstraZeneca (Sweden) · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAirway remodeling in COPD includes reorganization of the extracellular matrix. Proteoglycans play a crucial role in this process as regulators of the integrity of the extracellular matrix. Altered proteoglycan immunostaining has been demonstrated in COPD lungs and this has been suggested to contribute to the pathogenesis. The major cell type responsible for production and maintenance of ECM constituents, such as proteoglycans, are fibroblasts. Interestingly, it has been proposed that central airways and alveolar lung parenchyma contain distinct fibroblast populations. This study explores the hypothesis that altered depositions of proteoglycans in COPD lungs, and in particular versican and perlecan, is a result of dysregulated fibroblast proteoglycan production.

methodsProliferation, proteoglycan production and the response to TGF-beta1 were examined in vitro in centrally and distally derived fibroblasts isolated from COPD patients (GOLD stage IV) and from control subjects.

resultsPhenotypically different fibroblast populations were identified in central airways and in the lung parenchyma. Versican production was higher in distal fibroblasts from COPD patients than from control subjects (p < 0.01). In addition, perlecan production was lower in centrally derived fibroblasts from COPD patients than from control subjects (p < 0.01). TGF-beta1 triggered similar increases in proteoglycan production in distally derived fibroblasts from COPD patients and control subjects. In contrast, centrally derived fibroblasts from COPD patients were less responsive to TGF-beta1 than those from control subjects.

conclusionsThe results show that fibroblasts from COPD patients have alterations in proteoglycan production that may contribute to disease development. Distally derived fibroblasts from COPD patients have enhanced production of versican that may have a negative influence on the elastic recoil. In addition, a lower perlecan production in centrally derived fibroblasts from COPD patients may indicate alterations in bronchial basement membrane integrity in severe COPD.

Indexed as

AdultAgedBiglycanCase-Control StudiesCell ProliferationCells, CulturedDecorinExtracellular Matrix ProteinsFemaleFibroblastsHeparan Sulfate ProteoglycansHumansLungMaleMiddle AgedPhenotypeBGN protein, humanBiglycanDCN protein, humanDecorinExtracellular Matrix ProteinsHeparan Sulfate ProteoglycansperlecanProteoglycansTransforming Growth Factor beta1VCAN protein, humanVersicans

Identifiers

PMID20459817
PMCPMC2886021
OpenAlexW2049422998

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.