Evidence map›Paper›PMID 21791528›Full record

ArticleDevelopment (Cambridge, England)2011

Notch signaling prevents mucous metaplasia in mouse conducting airways during postnatal development.

Po-Nien Tsao, Shu-Chen Wei, Ming-Fang Wu, Miao-Tzu Huang, Hsien-Yi Lin, Ming-Cheng Lee, Kurt Ming-Chao Lin, I-Jong Wang, Vesa Kaartinen, Liang-Tung Yang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
7.5field-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

58 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Emerging cell and molecular targets for treating mucus hypersecretion in asthma.Allergology international : official journal of the Japanese Society of Allergology · 2024
    Review
  7. Article
  8. Review
  9. Lung Epithelial Cell Line Immune Responses toJournal of fungi (Basel, Switzerland) · 2023
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. LKB1 deficiency upregulates RELM-α to drive airway goblet cell metaplasia.Cellular and molecular life sciences : CMLS · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Notch Transduction in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2020
    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

11 authors at 2 institutions in 2 countries.

Po-Nien TsaoDepartment of Pediatrics, National Taiwan University Hospital, Taipei 100, Taiwan. tsaopn@ntu.edu.tw
Shu-Chen Wei
Ming-Fang Wu
Miao-Tzu Huang
Hsien-Yi Lin
Ming-Cheng Lee
Kurt Ming-Chao Lin
I-Jong Wang
Vesa Kaartinen
Liang-Tung Yang
Wellington V Cardoso
National Taiwan University Hospital · TWUniversity of Michigan–Ann Arbor · US

Funding

T1alpha in type I cell formation, regulation &functionP01HL047049 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FINE, ALAN FINE · 1992 to 2012
$27.6M
HSRD VA CDA 10-014NHLBI NIH HHS P01 HL047049NHLBI NIH HHS P01HL47049
6 · The paper itself

Abstract

Goblet cell metaplasia and mucus overproduction contribute to the pathogenesis of chronic lung diseases, including asthma and chronic obstructive pulmonary disease (COPD). Notch signaling regulates cell fate decisions and is crucial in controlling goblet cell differentiation in the gut epithelium. Little is known, however, about how endogenous Notch signaling influences the goblet cell differentiation program that takes place in the postnatal lung. Using a combination of genetic and in vitro approaches here we provide evidence of a novel role for Notch in restricting goblet cell differentiation in the airway epithelium during the postnatal period. Conditional inactivation of the essential Notch pathway component Pofut1 (protein O-fucosyltransferase1) in Tgfb3-Cre-expressing mice resulted in an aberrant postnatal airway phenotype characterized by marked goblet cell metaplasia, decreased Clara cell number and increase in ciliated cells. The presence of the same phenotype in mice in which the Notch transcriptional effector Rbpjk was deleted indicated the involvement of the canonical Notch pathway. Lineage study in vivo suggested that goblet cells originated from a subpopulation of Clara cells largely present in proximal airways in which Notch was disrupted. The phenotype was confirmed by a panel of goblet cell markers, showed no changes in cell proliferation or altered expression of proinflammatory cytokines and was associated with significant downregulation of the bHLH transcriptional repressor Hes5. Luciferase reporter analysis suggested that Notch directly repressed MUC5AC transcription in lung epithelial cells. The data suggested that during postnatal life Notch is required to prevent Clara cells from differentiating into goblet cells.

Indexed as

Signal TransductionAnimalsAnimals, NewbornBasic Helix-Loop-Helix ProteinsCell DifferentiationCytokinesDisease ProgressionFemaleFucosyltransferasesGene Expression Regulation, DevelopmentalLungMaleMetaplasiaMiceMucin 5ACReceptors, NotchBasic Helix-Loop-Helix ProteinsCytokinesFucosyltransferasesHes5 protein, mouseMuc5ac protein, mouseMucin 5ACPofut1 protein, mouseReceptors, NotchRepressor ProteinsTgfb3 protein, mouseTransforming Growth Factor beta3

Identifiers

PMID21791528
PMCPMC3148592
OpenAlexW2130208153

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.