Evidence map›Paper›PMID 29727583›Full record

ArticleAmerican journal of respiratory and critical care medicine2018

Protein Tyrosine Phosphatase-N13 Promotes Myofibroblast Resistance to Apoptosis in Idiopathic Pulmonary Fibrosis.

Alison Bamberg, Elizabeth F Redente, Steve D Groshong, Rubin M Tuder, Carlyne D Cool, Rebecca C Keith, Benjamin L Edelman, Bart P Black, Gregory P Cosgrove, Murry W Wynes and 5 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in American journal of respiratory and critical care medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  6. Mechanistic basis for the antifibrotic actions of cAMP-based therapies.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
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  11. Article
  12. Article
  13. CDKs Functional Analysis in Low Proliferating Early-Stage Pancreatic Ductal Adenocarcinoma.Journal of bioinformatics and systems biology : Open access · 2023
    Article
  14. Review
  15. Review
  16. CD148 Deficiency in Fibroblasts Promotes the Development of Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2021
    Article
  17. Article
  18. Article
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 6 institutions in 1 country.

Alison Bamberg1 Program in Cell Biology, Department of Pediatrics.
Elizabeth F Redente1 Program in Cell Biology, Department of Pediatrics.
Steve D Groshong5 Department of Medicine, and.
Rubin M Tuder3 Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, and.
Carlyne D Cool3 Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, and.
Rebecca C Keith5 Department of Medicine, and.
Benjamin L Edelman1 Program in Cell Biology, Department of Pediatrics.
Bart P Black1 Program in Cell Biology, Department of Pediatrics.
Gregory P Cosgrove5 Department of Medicine, and.
Murry W Wynes1 Program in Cell Biology, Department of Pediatrics.
Douglas Curran-Everett6 Division of Biostatistics and Bioinformatics, National Jewish Health, Denver, Colorado.
Stijn De Langhe7 Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama; and.
Luis A Ortiz8 Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, Pennsylvania.
Andrew Thorburn9 Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado.
David W H Riches1 Program in Cell Biology, Department of Pediatrics.
Pulmonary and Critical Care Associates · USVA Eastern Colorado Health Care System · USNational Jewish Health · USUniversity of Alabama at Birmingham · USUniversity of Colorado Denver · USUniversity of Pittsburgh · US

Funding

Fibroblast Resistance to Apoptosis in Pulmonary FibrosisR01HL140595 · NHLBI · NATIONAL JEWISH HEALTH · PI RICHES, DAVID W. · 2018 to 2021
$2.5M
HL-Lung stem cells and their niches.R01HL132156 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DE LANGHE, STIJN PIET JOHAN · 2016 to 2019
$2.0M
HL-Role of c-Myc in myofibroblast differentiation in pulmonary fibrosisR01HL126732 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DE LANGHE, STIJN PIET JOHAN, RICHES, DAVID W. · 2015 to 2018
$1.8M
DUSP1 as a therapeutic target in fibroproliferative acute lung injuryR01HL114754 · NHLBI · NATIONAL JEWISH HEALTH · PI RICHES, DAVID W. · 2013 to 2016
$1.6M
Therapeutic Targeting of PTPN13 in Idiopathic Pulmonary FibrosisI01BX003471 · VA · VA EASTERN COLORADO HEALTH CARE SYSTEM · PI RICHES, DAVID W. · 2017 to 2025
–
Mechanisms of TNF-alpha Mediated Resolution of Pulmonary FibrosisIK2BX002401 · VA · VA EASTERN COLORADO HEALTH CARE SYSTEM · PI REDENTE, ELIZABETH FRANCES · 2015 to 2019
–
BLRD VA I01 BX003471BLRD VA IK2 BX002401NHLBI NIH HHS R01 HL114754NHLBI NIH HHS R01 HL126732NHLBI NIH HHS R01 HL132156NHLBI NIH HHS R01 HL140595
6 · The paper itself

Abstract

rationaleIdiopathic pulmonary fibrosis (IPF) is a progressive, fibrotic interstitial lung disease characterized by (myo)fibroblast accumulation and collagen deposition. Resistance to Fas-induced apoptosis is thought to facilitate (myo)fibroblast persistence in fibrotic lung tissues by poorly understood mechanisms.

objectivesTo test the hypothesis that PTPN13 (protein tyrosine phosphatase-N13) is expressed by IPF lung (myo)fibroblasts, promotes their resistance to Fas-induced apoptosis, and contributes to the development of pulmonary fibrosis.

methodsPTPN13 was localized in lung tissues from patients with IPF and control subjects by immunohistochemical staining. Inhibition of PTPN13 function in primary IPF and normal lung (myo)fibroblasts was accomplished by: 1) downregulation with TNF-α (tumor necrosis factor-α)/IFN-γ, 2) siRNA knockdown, or 3) a cell-permeable Fas/PTPN13 interaction inhibitory peptide. The role of PTPN13 in the development of pulmonary fibrosis was assessed in mice with genetic deficiency of PTP-BL, the murine ortholog of PTPN13. MEASUREMENTS AND MAIN

resultsPTPN13 was constitutively expressed by (myo)fibroblasts in the fibroblastic foci of patients with IPF. Human lung (myo)fibroblasts, which are resistant to Fas-induced apoptosis, basally expressed PTPN13 in vitro. TNF-α/IFN-γ or siRNA-mediated PTPN13 downregulation and peptide-mediated inhibition of the Fas/PTPN13 interaction in human lung (myo)fibroblasts promoted Fas-induced apoptosis. Bleomycin-challenged PTP-BL

conclusionsThese findings suggest that PTPN13 mediates the resistance of human lung (myo)fibroblasts to Fas-induced apoptosis and promotes pulmonary fibrosis in mice. Our results suggest that strategies aimed at interfering with PTPN13 expression or function may represent a novel strategy to reduce fibrosis in IPF.

Indexed as

AnimalsApoptosisBiopsy, NeedleBleomycinCase-Control StudiesDown-RegulationDrug Resistance, Microbialfas ReceptorFemaleHumansIdiopathic Pulmonary FibrosisImmunohistochemistryMaleMiceMice, KnockoutMyofibroblastsBleomycinfas ReceptorProtein Tyrosine Phosphatase, Non-Receptor Type 13PTPN13 protein, humanRNA, Small Interferingapoptosis resistance(myo)fibroblastsPTPN13pulmonary fibrosis

Identifiers

PMID29727583
PMCPMC6173065
OpenAlexW2802141696

What OpenQuestion holds

Textmetadata
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Registered trials

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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.