Evidence map›Paper›PMID 9846974›Full record

ArticleThe American journal of pathology1998

TNF-alpha receptor knockout mice are protected from the fibroproliferative effects of inhaled asbestos fibers.

J Y Liu, D M Brass, G W Hoyle, A R Brody

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
9.0field-weighted citation impact, top 2% 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

56 citing papers in PubMed, 149 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. HMGB1 released by mesothelial cells drives the development of asbestos-induced mesothelioma.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  5. Article
  6. Review
  7. Review
  8. Observational
  9. Article
  10. Review
  11. Molecular and Clinical Features of EGFR-TKI-Associated Lung Injury.International journal of molecular sciences · 2021
    Review
  12. Obesity and the Development of Lung Fibrosis.Frontiers in pharmacology · 2021
    Review
  13. Review
  14. Article
  15. Patient with ankylosing spondylitis and scleroderma renal crisis.Mediterranean journal of rheumatology · 2018
    Article
  16. Article
  17. Article
  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

4 authors at 2 institutions in 1 country.

J Y LiuDepartment of Pathology, Tulane University Medical Center, New Orleans, Louisiana 70112-2699, USA.
D M Brass
G W Hoyle
A R Brody
Tulane University · USTulane Medical Center · US

Funding

TGF-B in Interstitial Lung DiseaseR01HL060532 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI BRODY, ARNOLD RALPH · 1997 to 2005
$1.9M
NHLBI NIH HHS R01 HL060532NHLBI NIH HHS R01HL60532NIEHS NIH HHS R01ES60766
6 · The paper itself

Abstract

We have demonstrated that C57BL/6-129 hybrid mice with genes for both the 55kd and 75kd receptors for TNF-alpha knocked out (TNF-alphaRKO) fail to develop fibroproliferative lesions after asbestos exposure. There is good evidence that TNF-alpha plays a major role in mediating interstitial pulmonary fibrosis. Our findings support this view and we present here new data obtained by in situ hybridization showing that expression of the genes coding for transforming growth factor alpha (TGF-alpha) and platelet-derived growth factor A-chain (PDGF-A) is reduced in the TNF-alphaRKO mice compared with control animals. In accordance with this observation, data on bromodeoxyuridine (BrdU) incorporation in the lungs of the TNF-alphaRKO mice show no increases over unexposed control animals. In contrast, wild-type control mice exposed to asbestos exhibit 15- to 20-fold increases in BrdU uptake and consequently develop fibrogenic lesions. Even though the levels of TNF-alpha gene expression and protein production were increased in the asbestos-exposed TNF-alphaRKO mice, the lack of receptor signaling protected the mice from developing fibroproliferative lesions. We agree with the view that TNF-alpha is essential for the development of interstitial pulmonary fibrosis and postulate that TNF-alpha mediates its effects through activation of other growth factors such as PDGF and TGF-alpha that control cell growth and matrix production.

Indexed as

AnimalsAsbestosCell DivisionImmunohistochemistryIn Situ HybridizationMiceMice, Inbred C57BLMice, KnockoutPlatelet-Derived Growth FactorPulmonary FibrosisReceptors, Tumor Necrosis FactorRNA, MessengerTransforming Growth Factor alphaTumor Necrosis Factor-alphaAsbestosPlatelet-Derived Growth FactorReceptors, Tumor Necrosis FactorRNA, MessengerTransforming Growth Factor alphaTumor Necrosis Factor-alpha

Identifiers

PMID9846974
PMCPMC1866331
OpenAlexW2071109600

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.