Evidence map›Paper›PMID 16763221›Full record

ArticleAmerican journal of respiratory cell and molecular biology2006

A3 adenosine receptor signaling contributes to airway mucin secretion after allergen challenge.

Hays W J Young, Chun-Xiao Sun, Christopher M Evans, Burton F Dickey, Michael R Blackburn

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 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Expression of adenosine receptors in monocytes from patients with bronchial asthma.Biochemical and biophysical research communications · 2015
    Article
  10. Article
  11. Review
  12. Article
  13. Gs-coupled adenosine receptors differentially limit antigen-induced mast cell activation.The Journal of pharmacology and experimental therapeutics · 2013
    Article
  14. Article
  15. Investigational A₃ adenosine receptor targeting agents.Expert opinion on investigational drugs · 2011
    Review
  16. Mucin production during prenatal and postnatal murine lung development.American journal of respiratory cell and molecular biology · 2011
    Article
  17. Adenosine receptors and vascular inflammation.Biochimica et biophysica acta · 2011
    Review
  18. Article
  19. Animal models of airway diseases.Sub-cellular biochemistry · 2011
    Review
  20. 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

5 authors at 1 institution in 1 country.

Hays W J YoungDepartment of Biochemistry and Molecular Biology, University of Texas Health Science Center at Houston, Medical School, 6431 Fannin, Houston, TX 77030, USA.
Chun-Xiao Sun
Christopher M Evans
Burton F Dickey
Michael R Blackburn
The University of Texas Health Science Center at Houston · US

Funding

Adenosine Signaling and Lung FibrosisR01HL070952 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BLACKBURN, MICHAEL R · 2002 to 2019
$5.7M
Molecular Models of Adenosine Signaling and AsthmaR01AI043572 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BLACKBURN, MICHAEL R · 1998 to 2008
$1.8M
Munc18 Proteins in Airway Mucus HypersecretionR01HL072984 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DICKEY, BURTON F · 2003 to 2006
$1.5M
NHLBI NIH HHS HL70952NHLBI NIH HHS HL72984NIAID NIH HHS AI43572
6 · The paper itself

Abstract

Mucin hypersecretion is a prominent feature of obstructive airway diseases such as asthma. Clara cells conditionally produce mucin in response to inflammatory signals in a process termed mucous metaplasia. This can be followed by mucin secretion stimulated by various signaling molecules. The cellular and molecular mechanisms that regulate mucin production and secretion are not well understood. Adenosine is a signaling nucleoside that has been implicated in airway diseases in which mucus obstruction is prominent. Furthermore, the A(3) adenosine receptor (A(3)AR) is upregulated in mucin-producing goblet cells of the airway, thereby implicating it in processes involved in mucous cell biology. Here we use genetic approaches to investigate the contribution of A(3)AR signaling to mucus production and secretion in a mouse model of allergen-induced pulmonary disease. We found that the degree of mucin production in response to allergen is similar in wild-type and A(3)AR-deficient mice, and that overexpression of this receptor in Clara cells neither induces mucin production itself, nor enhances mucin production in response to allergen challenge. Collectively, these experiments demonstrate that the A(3)AR is neither necessary nor sufficient for mucous cell metaplasia. In contrast to the lack of effect on mucin production, agonist-induced mucin secretion was increased in goblet cells overexpressing the A(3)AR, and was absent in A(3)AR-deficient mice. Thus, the A(3)AR contributes to mucin secretion in allergen-induced metaplasia. Signaling through this receptor may contribute to mucus airway obstruction seen in pulmonary disorders in which adenosine levels are elevated.

Indexed as

Bronchial Provocation TestsAnimalsCell ShapeMetaplasiaMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMucinsOvalbuminReceptor, Adenosine A3Respiratory MucosaSignal TransductionMucinsOvalbuminReceptor, Adenosine A3

Identifiers

PMID16763221
PMCPMC2643274
OpenAlexW2152178249

What Socratic 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 Socratic graph.