Evidence map›Paper›PMID 28056339›Full record

ArticleThe American journal of pathology2017

Asbestos-Induced Mesothelial to Fibroblastic Transition Is Modulated by the Inflammasome.

Joyce K Thompson, Maximilian B MacPherson, Stacie L Beuschel, Arti Shukla

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

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  15. Mesothelium and Malignant Mesothelioma.Journal of developmental biology · 2019
    Review
  16. Exosomes from asbestos-exposed cells modulate gene expression in mesothelial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  17. Article
  18. Article
  19. Review
  20. Targeting the epigenome in malignant pleural mesothelioma.Translational lung cancer research · 2017
    Review
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 1 institution in 1 country.

Joyce K ThompsonDepartment of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, Vermont.
Maximilian B MacPhersonDepartment of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, Vermont.
Stacie L BeuschelDepartment of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, Vermont.
Arti ShuklaDepartment of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, Vermont. Electronic address: arti.shukla@uvm.edu.
University of Vermont · US

Funding

Inflammasomes in pathogenesis of mesotheliomaR01ES021110 · NIEHS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI SHUKLA, ARTI · 2012 to 2016
$1.7M
NIEHS NIH HHS R01 ES021110
6 · The paper itself

Abstract

Despite the causal relationship established between malignant mesothelioma (MM) and asbestos exposure, the exact mechanism by which asbestos induces this neoplasm and other asbestos-related diseases is still not well understood. MM is characterized by chronic inflammation, which is believed to play an intrinsic role in the origin of this disease. We recently found that asbestos activates the nod-like receptor family member containing a pyrin domain 3 (NLRP3) inflammasome in a protracted manner, leading to an up-regulation of IL-1β and IL-18 production in human mesothelial cells. Combined with biopersistence of asbestos fibers, we hypothesize that this creates an environment of chronic IL-1β signaling in human mesothelial cells, which may promote mesothelial to fibroblastic transition (MFT) in an NLRP3-dependent manner. Using a series of experiments, we found that asbestos induces a fibroblastic transition of mesothelial cells with a gain of mesenchymal markers (vimentin and N-cadherin), whereas epithelial markers, such as E-cadherin, are down-regulated. Use of siRNA against NLRP3, recombinant IL-1β, and IL-1 receptor antagonist confirmed the role of NLRP3 inflammasome-dependent IL-1β in the process. In vivo studies using wild-type and various inflammasome component knockout mice also revealed the process of asbestos-induced mesothelial to fibroblastic transition and its amelioration in caspase-1 knockout mice. Taken together, our data are the first to suggest that asbestos induces mesothelial to fibroblastic transition in an inflammasome-dependent manner.

Indexed as

AnimalsAsbestosBiomarkersCaspase 1Cell LineCell ShapeEpithelial CellsEpitheliumFibroblastsGene Expression ProfilingGene Expression RegulationHumansInflammasomesInterleukin-1betaMiceNLR Family, Pyrin Domain-Containing 3 ProteinAsbestosBiomarkersCaspase 1InflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, human

Identifiers

PMID28056339
PMCPMC5389358
OpenAlexW2570671245

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.