Evidence map›Paper›PMID 23406566›Full record

ArticleRespiratory research2013

Defective alterations in the collagen network to prostacyclin in COPD lung fibroblasts.

Anna-Karin Larsson-Callerfelt, Oskar Hallgren, Annika Andersson-Sjöland, Lena Thiman, Johan Björklund, Josefine Kron, Kristian Nihlberg, Leif Bjermer, Claes-Göran Löfdahl, Gunilla Westergren-Thorsson

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.6field-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

14 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Small airway fibroblasts from patients with chronic obstructive pulmonary disease exhibit cellular senescence.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Lung ageing and COPD: is there a role for ageing in abnormal tissue repair?European respiratory review : an official journal of the European Respiratory Society · 2017
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. 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

10 authors at 1 institution in 1 country.

Anna-Karin Larsson-CallerfeltUnit of Lung Biology, Department of Experimental Medical Sciences, BMC D12, Lund University, Lund 221 84, Sweden. Anna-Karin_L.Larsson@med.lu.se
Oskar Hallgren
Annika Andersson-Sjöland
Lena Thiman
Johan Björklund
Josefine Kron
Kristian Nihlberg
Leif Bjermer
Claes-Göran Löfdahl
Gunilla Westergren-Thorsson
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProstacyclin analogs are potent vasodilators and possess anti-inflammatory properties. However, the effect of prostacyclin on extracellular matrix (ECM) in COPD is not well known. Collagen fibrils and proteoglycans are essential ECM components in the lung and fibroblasts are key players in regulating the homeostasis of ECM proteins. The aim was to study the synthesis of prostacyclin and its effect on fibroblast activity and ECM production, and in particular collagen I and the collagen-associated proteoglycans biglycan and decorin.

methodsParenchymal lung fibroblasts were isolated from lungs from COPD patients (GOLD stage IV) and from lungs and transbronchial biopsies from control subjects. The prostacyclin analog iloprost was used to study the effect of prostacyclin on ECM protein synthesis, migration, proliferation and contractile capacity of fibroblasts.

resultsTGF-β1 stimulation significantly increased prostacyclin synthesis in fibroblasts from COPD patients (p < 0.01), but showed no effect on fibroblasts from control subjects. Collagen I synthesis was decreased by iloprost in both control and COPD fibroblasts (p < 0.05). Conversely, iloprost significantly altered biglycan and decorin synthesis in control fibroblasts, but iloprost displayed no effect on these proteoglycans in COPD fibroblasts. Proliferation rate was reduced (p < 0.05) and contractile capacity was increased in COPD fibroblasts (p < 0.05) compared to control fibroblasts. Iloprost decreased proliferative rate in control fibroblasts (p < 0.05), whereas iloprost attenuated contraction capacity in both COPD (p < 0.01) and control fibroblasts (p < 0.05).

conclusionsIloprost reduced collagen I synthesis and fibroblast contractility but did not affect the collagen-associated proteoglycans or proliferation rate in fibroblasts from COPD patients. Enhanced prostacyclin production could lead to improper collagen network fibrillogenesis and a more emphysematous lung structure in severe COPD patients.

Indexed as

AdultBiglycanBiopsyCase-Control StudiesCell MovementCell ProliferationCells, CulturedCollagen Type IDecorinEpoprostenolFemaleFibroblastsHumansIloprostLungMaleBGN protein, humanBiglycanCollagen Type IDCN protein, humanDecorinEpoprostenolIloprostTGFB1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID23406566
PMCPMC3585859
OpenAlexW1967202916

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.