Evidence map›Paper›PMID 22493011›Full record

ArticleAmerican journal of respiratory cell and molecular biology2012

Amphiregulin-dependent mucous cell metaplasia in a model of nonallergic lung injury.

Nicholas D Manzo, W Michael Foster, Barry R Stripp

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Cell Culture Differentiation and Proliferation Conditions Influence theAmerican journal of respiratory cell and molecular biology · 2024
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  16. IL-33 promotes an innate immune pathway of intestinal tissue protection dependent on amphiregulin-EGFR interactions.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  17. Article
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  19. Article
  20. Human neutrophil elastase-mediated goblet cell metaplasia is attenuated in TACE-deficient mice.American journal of physiology. Lung cellular and molecular physiology · 2013
    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.

Nicholas D ManzoDivision of Pulmonary, Allergy and Critical Care, Duke University Medical Center, Durham, North Carolina, USA.
W Michael Foster
Barry R Stripp
Duke Medical Center · USDuke University · US

Funding

INTERDISCIPLINARY TRAINING PROGRAM IN LUNG DISEASET32HL007538 · NHLBI · DUKE UNIVERSITY · PI LEE, PATTY J, PALMER, SCOTT M · 1985 to 2019
$7.2M
STEM CELLS IN AIRWAY REPAIRR01HL064888 · NHLBI · UNIVERSITY OF ROCHESTER · PI STRIPP, BARRY R · 2000 to 2009
$3.1M
Stem Cells to Enhance Bronchiolar Reparative Capacity.R01HL090146 · NHLBI · DUKE UNIVERSITY · PI STRIPP, BARRY R · 2007 to 2010
$2.6M
Dependency of O-3 Induced Lung Mucus Hypersecretion on NQ01R01ES016347 · NIEHS · DUKE UNIVERSITY · PI FOSTER, W MICHAEL · 2008 to 2010
$1.0M
NHLBI NIH HHS 5R01HL064888-10NHLBI NIH HHS 5R01HL090146-04NHLBI NIH HHS 5T32HL007538-27NHLBI NIH HHS R01 HL064888NHLBI NIH HHS R01 HL090146NHLBI NIH HHS T32 HL007538NIEHS NIH HHS 5R01ES016347NIEHS NIH HHS R01 ES016347
6 · The paper itself

Abstract

Proliferation and differentiation of the pulmonary epithelium after injury is a critical process in the defense against the external environment. Defects in this response can result in airway remodeling, such as mucus cell metaplasia (MCM), commonly seen in patients with chronic lung disease. We have previously shown that amphiregulin (AREG), a ligand to the epidermal growth factor receptor (EGFR), is induced during the repair/differentiation process elicited by naphthalene-induced lung injury. Thus, we hypothesized that AREG signaling plays an important role in epithelial proliferation and differentiation of the repairing airway. Mice deficient in AREG and lung epithelial EGFR were used to define roles for AREG-dependent EGFR signaling in airway repair and remodeling. We show that AREG and epithelial EGFR expression is dispensable to pulmonary epithelial repair after naphthalene-induced lung injury, but regulates secretory cell differentiation to a mucus-producing phenotype. We show that the pulmonary epithelium is the source of AREG, suggesting that naphthalene-induced MCM is mediated through an autocrine signaling mechanism. However, induction of MCM resulting from allergen exposure was independent of AREG. Our data demonstrate that AREG-dependent EGFR signaling in airway epithelial cells contributes to MCM in naphthalene-induced lung injury. We conclude that AREG may represent a determinant of nonallergic chronic lung diseases complicated by MCM.

Indexed as

AmphiregulinAnimalsCell DifferentiationEGF Family of ProteinsErbB ReceptorsFemaleFlow CytometryGlycoproteinsIntercellular Signaling Peptides and ProteinsLung InjuryMetaplasiaMiceMucous MembraneReal-Time Polymerase Chain ReactionSignal TransductionAmphiregulinAreg protein, mouseEGF Family of ProteinsErbB ReceptorsGlycoproteinsIntercellular Signaling Peptides and Proteins

Identifiers

PMID22493011
PMCPMC3488692
OpenAlexW2113114650

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.