Evidence map›Paper›PMID 16424381›Full record

ArticleAmerican journal of respiratory cell and molecular biology2006

Epidermal growth factor receptor activation by epidermal growth factor mediates oxidant-induced goblet cell metaplasia in human airway epithelium.

S Marina Casalino-Matsuda, Maria E Monzón, Rosanna M Forteza

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
6.9field-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

77 citing papers in PubMed, 165 citations in OpenAlex.

  1. Trial
  2. Microbiology spectrum · 2026
    Article
  3. Review
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  15. Article
  16. Methods for isolating and analyzing physiological hyaluronan: a review.American journal of physiology. Cell physiology · 2022
    Review
  17. Review
  18. Article
  19. Article
  20. Role and mechanisms of autophagy in lung metabolism and repair.Cellular and molecular life sciences : CMLS · 2021
    Review

17 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

S Marina Casalino-MatsudaDivision of Pulmonary and Critical Care Medicine (R-47), University of Miami School of Medicine, 1600 NW 10th Ave, RMSB 7072A, Miami, FL 33136, USA. mmatsuda@med.miami.edu
Maria E Monzón
Rosanna M Forteza
University of Miami · US

Funding

MECHANISMS OF OXIDANT-INDUCED CHRONIC BRONCHITISR01HL073156 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MALBRAN FORTEZA, ROSANNA C · 2003 to 2012
$2.8M
THE ROLE OF HYALURONAN IN AIRWAY HYPERREACTIVITYR01HL068992 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MALBRAN FORTEZA, ROSANNA C · 2002 to 2005
$1.1M
NHLBI NIH HHS HL-073156NHLBI NIH HHS HL-68992
6 · The paper itself

Abstract

Mucus overproduction in inflammatory and obstructive airway diseases is associated with goblet cell (GC) metaplasia in airways. Although the mechanisms involved in GC metaplasia and mucus hypersecretion are not completely understood, association with oxidative stress and epidermal growth factor receptor (EGFR) signaling has been reported. To explore the mechanisms involved in oxidative stress-induced GC metaplasia, cultures of differentiated normal human bronchial epithelial cells grown at the air-liquid interface were exposed to reactive oxygen species (ROS) generated by xanthine/xanthine oxidase. EGFR activation and signaling was assessed by measuring EGF and transforming growth factor-alpha release and EGFR and (44/42)MAPK phosphorylation. The GC population was evaluated by confocal microscopy. ROS-induced EGFR activation resulted in GC proliferation and increased MUC5AC gene and protein expression. Signaling was due to pro-EGF processing by tissue kallikrein (TK), which was activated by ROS-induced hyaluronan breakdown. It was inhibited by catalase, a TK inhibitor, and EGF-blocking antibodies. Exposure to recombinant TK mimicked the ROS effects, increasing the expression of MUC5AC and lactoperoxidase. In addition, ROS induced the antiapoptotic factor Bcl-2 in a TK-dependent fashion. In conclusion, ROS-induced GC metaplasia in normal human bronchial epithelial cells is associated with HA depolymerization and EGF processing by TK followed by EGFR signaling, suggesting that increases in TK activity could contribute to GC metaplasia and mucus hypersecretion in diseases such as asthma and chronic bronchitis. The data also suggest that increases in GC population could be sustained by the associated upregulation of Bcl-2 in airway epithelial cells.

Indexed as

Cell DifferentiationCell ProliferationEpidermal Growth FactorEpithelial CellsErbB ReceptorsGoblet CellsHumansHyaluronic AcidLactoperoxidaseMetaplasiaMucin 5ACMucinsOxidantsOxidative StressPolymersProtein PrecursorsEpidermal Growth Factorepidermal growth factor precursorErbB ReceptorsHyaluronic AcidLactoperoxidaseMUC5AC protein, humanMucin 5ACMucinsOxidantsPolymersProtein PrecursorsProto-Oncogene Proteins c-bcl-2RNA, MessengerTissue KallikreinsXanthine Oxidase

Identifiers

PMID16424381
PMCPMC2644222
OpenAlexW2118755647

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.