Evidence map›Paper›PMID 21039988›Full record

ArticleInternational journal of experimental pathology2011

Oxidative damage and TGF-β differentially induce lung epithelial cell sonic hedgehog and tenascin-C expression: implications for the regulation of lung remodelling in idiopathic interstitial lung disease.

Paul M Fitch, Sarah E M Howie, William A H Wallace

Open access · greenAbstract read
In one paragraph

Article in International journal of experimental pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.9field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Aberrant Multiciliogenesis in Idiopathic Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022
    Article
  6. Review
  7. Review
  8. Article
  9. CGRP: A New Endogenous Cell Stemness Maintenance Molecule.Oxidative medicine and cellular longevity · 2022
    Review
  10. Review
  11. Review
  12. Immunohistochemical Comparative Study of Aggressive and Non-aggressive Central Giant Cell Lesions of the Jaws Based on the Tenascin-C Expression Profile.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

3 authors at 2 institutions in 1 country.

Paul M FitchMRC Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh, UK. pfitch@staffmail.ed.ac.uk
Sarah E M Howie
William A H Wallace
Queen's Medical Centre · GBEdinburgh Royal Infirmary · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic interstitial lung diseases (iILDs) are characterized by inflammation, hyperplasia of Type-II alveolar epithelial cells (AECs) and lung remodelling often with progressive fibrosis. It remains unclear which signals initiate iILD and/or maintain the disease processes. Using real-time RT-PCR and immunohistochemistry on archival biopsies of three patterns of iILD (usual interstitial pneumonitis/UIP, non-specific interstitial pneumonitis/NSIP and cryptogenic organizing pneumonia/COP) we investigated whether hedgehog signalling (previously associated with lung damage and repair) was functional and whether the damage associated extracellular matrix protein tenascin-C was present in activated Type-II AECs in all three iILDs. Using tissue culture, protein and mRNA detection we also determined how two signals (oxidative damage and TGF-β) associated with iILD pathogenesis affected Sonic hedgehog (SHH) and tenascin-C production by a Type-II AEC cell line. We report that SHH pathway and tenascin-C mRNA and proteins were found in UIP, NSIP and COP. SHH signalling was most active at sites of immature organizing fibrous tissue (fibroblastic foci) in UIP. In vitro Type-II AECs constitutively secrete SHH but not tenascin-C. Oxidative injury stimulated SHH release whereas TGF-β inhibited it. TGF-β and oxidative damage both upregulated tenascin-C mRNA but only TGF-β induced synthesis and release of a distinct protein isoform. SHH signalling is active in Type-II AECs from three types of ILD and all three express tenascin-C.

Indexed as

AdultAgedBlotting, WesternEpithelial CellsFemaleHedgehog ProteinsHumansImmunohistochemistryLung Diseases, InterstitialMaleMiddle AgedOxidative StressRespiratory MucosaReverse Transcriptase Polymerase Chain ReactionSignal TransductionTenascinHedgehog ProteinsSHH protein, humanTenascinTransforming Growth Factor beta

Identifiers

PMID21039988
PMCPMC3052752
OpenAlexW1486041442

What OpenQuestion holds

Textmetadata
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.