Evidence map›Paper›PMID 20429916›Full record

ArticleRespiratory research2010

Cigarette smoke and lipopolysaccharide induce a proliferative airway smooth muscle phenotype.

Tonio Pera, Reinoud Gosens, Andries H Lesterhuis, Riham Sami, Marco van der Toorn, Johan Zaagsma, Herman Meurs

Open access · goldAbstract read
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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 69 citations in OpenAlex.

  1. Cigarette smoke enhances proliferation and extracellular matrix deposition by human fetal airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2014
    Trial
  2. [Overexpressing NDUFA13 and CRIP1 improves B cell injury and lung Lesions in COPD mouse models].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
  3. Review
  4. Review
  5. Airway Smooth Muscle Regulated by Oxidative Stress in COPD.Antioxidants (Basel, Switzerland) · 2023
    Review
  6. Article
  7. Article
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  9. Epigenetic Links to Airway Smooth Muscle Proliferation.American journal of respiratory cell and molecular biology · 2019
    Article
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  11. Article
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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

7 authors at 2 institutions in 1 country.

Tonio PeraDepartment of Molecular Pharmacology, University Centre for Pharmacy, University of Groningen, Groningen, The Netherlands. t.pera@rug.nl
Reinoud Gosens
Andries H Lesterhuis
Riham Sami
Marco van der Toorn
Johan Zaagsma
Herman Meurs
University of Groningen · NLUniversity Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA major feature of chronic obstructive pulmonary disease (COPD) is airway remodelling, which includes an increased airway smooth muscle (ASM) mass. The mechanisms underlying ASM remodelling in COPD are currently unknown. We hypothesized that cigarette smoke (CS) and/or lipopolysaccharide (LPS), a major constituent of CS, organic dust and gram-negative bacteria, that may be involved in recurrent airway infections and exacerbations in COPD patients, would induce phenotype changes of ASM.

methodsTo this aim, using cultured bovine tracheal smooth muscle (BTSM) cells and tissue, we investigated the direct effects of CS extract (CSE) and LPS on ASM proliferation and contractility.

resultsBoth CSE and LPS induced a profound and concentration-dependent increase in DNA synthesis in BTSM cells. CSE and LPS also induced a significant increase in BTSM cell number, which was associated with increased cyclin D1 expression and dependent on activation of ERK 1/2 and p38 MAP kinase. Consistent with a shift to a more proliferative phenotype, prolonged treatment of BTSM strips with CSE or LPS significantly decreased maximal methacholine- and KCl-induced contraction.

conclusionsDirect exposure of ASM to CSE or LPS causes the induction of a proliferative, hypocontractile ASM phenotype, which may be involved in airway remodelling in COPD.

Indexed as

Airway RemodelingAnimalsCattleCell ProliferationCells, CulturedCyclin D1DNA ReplicationDose-Response Relationship, DrugFlavonoidsImidazolesIsometric ContractionLipopolysaccharidesMethacholine ChlorideMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Muscle, Smooth2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneCyclin D1FlavonoidsImidazoleslipopolysaccharide, E coli O55-B5LipopolysaccharidesMethacholine ChlorideMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3p38 Mitogen-Activated Protein KinasesPotassium ChlorideProtein Kinase InhibitorsPyrimidinesSB 239063Smoke

Identifiers

PMID20429916
PMCPMC2873257
OpenAlexW2146405971

What OpenQuestion holds

Textmetadata
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.