Evidence map›Paper›PMID 30230348›Full record

ArticleAmerican journal of respiratory cell and molecular biology2019

P311 Promotes Lung Fibrosis via Stimulation of Transforming Growth Factor-β1, -β2, and -β3 Translation.

Fang-Fang Duan, Gabriel Barron, Angelo Meliton, Gokhan M Mutlu, Nickolai O Dulin, Lucia Schuger

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Regulation of inflammatory lung injury and repair by transforming growth factors.American journal of physiology. Lung cellular and molecular physiology · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
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  11. Article
  12. Article
  13. Article
  14. Common and Rare Genetic Variants That Could Contribute to Severe Otitis Media in an Australian Aboriginal Population.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Update in Interstitial Lung Disease 2019.American journal of respiratory and critical care medicine · 2020
    Review
  19. Impaired Myofibroblast Dedifferentiation Contributes to Nonresolving Fibrosis in Aging.American journal of respiratory cell and molecular biology · 2020
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Fang-Fang Duan1 Department of Pathology and.
Gabriel Barron1 Department of Pathology and.
Angelo Meliton2 Section of Pulmonary and Critical Care Medicine, Department of Medicine, The University of Chicago Medical School, Chicago, Illinois.
Gokhan M Mutlu2 Section of Pulmonary and Critical Care Medicine, Department of Medicine, The University of Chicago Medical School, Chicago, Illinois.
Nickolai O Dulin2 Section of Pulmonary and Critical Care Medicine, Department of Medicine, The University of Chicago Medical School, Chicago, Illinois.
Lucia Schuger1 Department of Pathology and.
University of Chicago · US

Funding

P311 in Pulmonary RepairR01HL132870 · NHLBI · UNIVERSITY OF CHICAGO · PI SCHUGER, LUCIA · 2016 to 2019
$1.6M
NHLBI NIH HHS R01 HL132870
6 · The paper itself

Abstract

Interstitial lung fibrosis, a frequently idiopathic and fatal disease, has been linked to the increased expression of profibrotic transforming growth factor (TGF)-βs. P311 is an RNA-binding protein that stimulates TGF-β1, -β2, and -β3 translation in several cell types through its interaction with the eukaryotic translation initiation factor 3b. We report that P311 is switched on in the lungs of patients with idiopathic pulmonary fibrosis (IPF) and in the mouse model of bleomycin (BLM)-induced pulmonary fibrosis. To assess the in vivo role of P311 in lung fibrosis, BLM was instilled into the lungs of P311-knockout mice, in which fibrotic changes were significantly decreased in tandem with a reduction in TGF-β1, -β2, and -β3 concentration/activity compared with BLM-treated wild-type mice. Complementing these findings, forced P311 expression increased TGF-β concentration/activity in mouse and human lung fibroblasts, thereby leading to an activated phenotype with increased collagen production, as seen in IPF. Consistent with a specific effect of P311 on TGF-β translation, TGF-β1-, -β2-, and -β3-neutralizing antibodies downregulated P311-induced collagen production by lung fibroblasts. Furthermore, treatment of BLM-exposed P311 knockouts with recombinant TGF-β1, -β2, and -β3 induced pulmonary fibrosis to a degree similar to that found in BLM-treated wild-type mice. These studies demonstrate the essential function of P311 in TGF-β-mediated lung fibrosis. Targeting P311 could prove efficacious in ameliorating the severity of IPF while circumventing the development of autoimmune complications and toxicities associated with the use of global TGF-β inhibitors.

Indexed as

AnimalsBleomycinCase-Control StudiesCollagenDisease Models, AnimalFibroblastsHumansIdiopathic Pulmonary FibrosisMaleMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsOncogene ProteinsProtein BiosynthesisPulmonary FibrosisTransforming Growth Factor beta1BleomycinCollagenNerve Tissue ProteinsNREP protein, humanOncogene ProteinsP311 protein, mouseTgfb2 protein, mouseTransforming Growth Factor beta1Transforming Growth Factor beta2Transforming Growth Factor beta3bleomycinfibroblastslung fibrosisP311transforming growth factor-β

Identifiers

PMID30230348
PMCPMC6376409
OpenAlexW2892243262

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.