Evidence map›Paper›PMID 14718259›Full record

ArticleBritish journal of pharmacology2004

PPAR gamma ligands, 15-deoxy-delta12,14-prostaglandin J2 and rosiglitazone regulate human cultured airway smooth muscle proliferation through different mechanisms.

Jane E Ward, Haslinda Gould, Trudi Harris, John V Bonacci, Alastair G Stewart

Registry-linked trialOpen access · bronzeAbstract readComparative Study
In one paragraph

Article in British journal of pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00614874 (The Effects of the PPARy Agonist Rosiglitazone on Airway Hyperreactivity), which is not on this map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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.

NCT00614874 phase2completednot on this mapstarted 2008, after this paper: background citation

The Effects of the PPARy Agonist Rosiglitazone on Airway Hyperreactivity

TypeinterventionalSponsorCreighton UniversityRan2008 to 2010Enrolled16ConditionsAsthmaArmsrosiglitazone
3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. 15-Deoxy-Delta-12,14-Prostaglandin JFrontiers in immunology · 2017
    Article
  8. Article
  9. 15-Deoxy-ΔFrontiers in immunology · 2016
    Article
  10. Article
  11. Novel small airway bronchodilator responses to rosiglitazone in mouse lung slices.American journal of respiratory cell and molecular biology · 2014
    Article
  12. Treatment of etoposide combined with 15-deoxy-ΔMolecular and clinical oncology · 2014
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

5 authors at 1 institution in 1 country.

Jane E WardDepartment of Pharmacology, University of Melbourne, Melbourne, Victoria 3010, Australia. janeew@unimelb.edu.au
Haslinda Gould
Trudi Harris
John V Bonacci
Alastair G Stewart
University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The influence of two peroxisome proliferator-activated receptor gamma (PPARgamma) ligands, a thiazolidinedione, rosiglitazone (RG) and the prostaglandin D2 metabolite 15-deoxy-Delta(12,14)-prostaglandin J2 (15d-PGJ2) on the proliferation of human cultured airway smooth muscle (HASM) was examined. The increases in HASM cell number in response to basic fibroblast growth factor (bFGF, 300 pm) or thrombin (0.3 U ml-1) were significantly inhibited by either RG (1-10 microM) or 15d-PGJ2 (1-10 microM). The effects of RG, but not 15d-PGJ2, were reversed by the selective PPARgamma antagonist GW9662 (1 microM). Neither RG nor 15d-PGJ2 (10 microM) decreased cell viability, or induced apoptosis, suggesting that the regulation of cell number was due to inhibition of proliferation, rather than increased cell death. Flow-cytometric analysis of HASM cell cycle distribution 24 h after bFGF addition showed that RG prevented the progression of cells from G1 to S phase. In contrast, 15d-PGJ2 caused an increase in the proportion of cells in S phase, and a decrease in G2/M, compared to bFGF alone. Neither RG nor 15d-PGJ2 inhibited ERK phosphorylation measured 6 h post mitogen addition. The bFGF-mediated increase in cyclin D1 protein levels after 8 h was reduced in the presence of 15d-PGJ2, but not RG. Although both RG and 15d-PGJ2 can inhibit proliferation of HASM irrespective of the mitogen used, only the antiproliferative effects of RG appear to be PPARgamma-dependent. The different antimitogenic mechanisms of 15d-PGJ2 and synthetic ligands for PPARgamma may be exploited to optimise the potential for these compounds to inhibit airway remodelling in asthma. British Journal of Pharmacology (2004) 141, 517-525. doi:10.1038/sj.bjp.0705630

Indexed as

BronchiCell CountCell DivisionCells, CulturedHumansLigandsMuscle, SmoothProstaglandin D2Receptors, Cytoplasmic and NuclearRosiglitazoneThiazolidinedionesTranscription Factors15-deoxyprostaglandin J2LigandsProstaglandin D2Receptors, Cytoplasmic and NuclearRosiglitazoneThiazolidinedionesTranscription Factors

Identifiers

PMID14718259
PMCPMC1574213
OpenAlexW2049018801

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.