Evidence map›Paper›PMID 24587395›Full record

ArticlePloS one2014

Extra-cellular matrix proteins induce matrix metalloproteinase-1 (MMP-1) activity and increase airway smooth muscle contraction in asthma.

Natasha K Rogers, Debbie Clements, Arundhati Dongre, Tim W Harrison, Dominic Shaw, Simon R Johnson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
1.1field-weighted citation impact, top 24% 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, 42 citations in OpenAlex.

  1. Deciphering the Tenascin-C Nexus: A Comprehensive Review of Its Involvement in Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review
  2. Review
  3. Article
  4. Article
  5. Article
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  7. Article
  8. Review
  9. Review
  10. Sustained exposure to prostaglandin DJournal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2019
    Article
  11. Article
  12. Article
  13. Fibroblast-to-myofibroblast transition in bronchial asthma.Cellular and molecular life sciences : CMLS · 2018
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Mechanisms of airway hyper-responsiveness in asthma: the past, present and yet to come.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2015
    Review
  20. Article
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

6 authors at 1 institution in 1 country.

Natasha K RogersDivision of Respiratory Medicine and Respiratory Research Unit, University of Nottingham, Nottingham, England, United Kingdom.
Debbie ClementsDivision of Respiratory Medicine and Respiratory Research Unit, University of Nottingham, Nottingham, England, United Kingdom.
Arundhati DongreDivision of Respiratory Medicine and Respiratory Research Unit, University of Nottingham, Nottingham, England, United Kingdom.
Tim W HarrisonDivision of Respiratory Medicine and Respiratory Research Unit, University of Nottingham, Nottingham, England, United Kingdom.
Dominic ShawDivision of Respiratory Medicine and Respiratory Research Unit, University of Nottingham, Nottingham, England, United Kingdom.
Simon R JohnsonDivision of Respiratory Medicine and Respiratory Research Unit, University of Nottingham, Nottingham, England, United Kingdom.
University of Nottingham · GB

Funding

Medical Research Council G1100163
6 · The paper itself

Abstract

Airway remodelling describes the histopathological changes leading to fixed airway obstruction in patients with asthma and includes extra-cellular matrix (ECM) deposition. Matrix metalloproteinase-1 (MMP-1) is present in remodelled airways but its relationship with ECM proteins and the resulting functional consequences are unknown. We used airway smooth muscle cells (ASM) and bronchial biopsies from control donors and patients with asthma to examine the regulation of MMP-1 by ECM in ASM cells and the effect of MMP-1 on ASM contraction. Collagen-I and tenascin-C induced MMP-1 protein expression, which for tenascin-C, was greater in asthma derived ASM cells. Tenascin-C induced MMP-1 expression was dependent on ERK1/2, JNK and p38 MAPK activation and attenuated by function blocking antibodies against the β1 and β3 integrin subunits. Tenascin-C and MMP-1 were not expressed in normal airways but co-localised in the ASM bundles and reticular basement membrane of patients with asthma. Further, ECM from asthma derived ASM cells stimulated MMP-1 expression to a greater degree than ECM from normal ASM. Bradykinin induced contraction of ASM cells seeded in 3D collagen gels was reduced by the MMP inhibitor ilomastat and by siRNA knockdown of MMP-1. In summary, the induction of MMP-1 in ASM cells by tenascin-C occurs in part via integrin mediated MAPK signalling. MMP-1 and tenascin-C are co-localised in the smooth muscle bundles of patients with asthma where this interaction may contribute to enhanced airway contraction. Our findings suggest that ECM changes in airway remodelling via MMP-1 could contribute to an environment promoting greater airway narrowing in response to broncho-constrictor stimuli and worsening asthma symptoms.

Indexed as

AsthmaBradykininCells, CulturedCollagen Type IDose-Response Relationship, DrugExtracellular MatrixExtracellular Matrix ProteinsGene ExpressionHumansHydroxamic AcidsImmunoblottingIndolesIntegrin beta1Integrin beta3Matrix Metalloproteinase 1Mitogen-Activated Protein KinasesBradykininCollagen Type IExtracellular Matrix ProteinsHydroxamic AcidsilomastatIndolesIntegrin beta1Integrin beta3Matrix Metalloproteinase 1Mitogen-Activated Protein KinasesTenascinVasodilator Agents

Identifiers

PMID24587395
PMCPMC3938782
OpenAlexW2039794214

What OpenQuestion holds

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LicenceCC BY
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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.