Evidence map›Paper›PMID 21984570›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012

Allergic inflammation induces a persistent mechanistic switch in thromboxane-mediated airway constriction in the mouse.

Jaime M Cyphert, Irving C Allen, Rachel J Church, Anne M Latour, John N Snouwaert, Thomas M Coffman, Beverly H Koller

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 37% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Thromboxane AAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. A Thromboxane AArteriosclerosis, thrombosis, and vascular biology · 2022
    Article
  9. Leukotriene BHeliyon · 2021
    Article
  10. Review
  11. 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

7 authors at 3 institutions in 2 countries.

Jaime M CyphertCurriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7264, USA.
Irving C Allen
Rachel J Church
Anne M Latour
John N Snouwaert
Thomas M Coffman
Beverly H Koller
Institut thématique Génétique, génomique et bioinformatique · FRUniversity of North Carolina at Chapel Hill · USDuke Medical Center · US

Funding

PGE2 in the Pathogenesis of Allergic Airways DiseaseR01HL068141 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KOLLER, BEVERLY H · 2001 to 2009
$3.2M
Eicosanoids and GPCRs in Airway PhysiologyR01HL080697 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KOLLER, BEVERLY H · 2006 to 2009
$1.4M
NHLBI NIH HHS HL-080697NHLBI NIH HHS R01HL-068141
6 · The paper itself

Abstract

Actions of thromboxane (TXA(2)) to alter airway resistance were first identified over 25 years ago. However, the mechanism underlying this physiological response has remained largely undefined. Here we address this question using a novel panel of mice in which expression of the thromboxane receptor (TP) has been genetically manipulated. We show that the response of the airways to TXA(2) is complex: it depends on expression of other G protein-coupled receptors but also on the physiological context of the signal. In the healthy airway, TXA(2)-mediated airway constriction depends on expression of TP receptors by smooth muscle cells. In contrast, in the inflamed lung, the direct actions of TXA(2) on smooth muscle cell TP receptors no longer contribute to bronchoconstriction. Instead, in allergic lung disease, TXA(2)-mediated airway constriction depends on neuronal TP receptors. Furthermore, this mechanistic switch persists long after resolution of pulmonary inflammation. Our findings demonstrate the powerful ability of lung inflammation to modify pathways leading to airway constriction, resulting in persistent changes in mechanisms of airway reactivity to key bronchoconstrictors. Such alterations are likely to shape the pathogenesis of asthmatic lung disease.

Indexed as

BronchoconstrictionMyocytes, Smooth MuscleNeurons, Afferent15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic AcidAirway ResistanceAnimalsAsthmaBronchiCells, CulturedHypersensitivityMiceMice, TransgenicPneumoniaReceptors, ThromboxaneReceptors, Thromboxane A2, Prostaglandin H2Respiratory System15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic AcidReceptors, ThromboxaneReceptors, Thromboxane A2, Prostaglandin H2Thromboxane A2Vasoconstrictor Agents

Identifiers

PMID21984570
PMCPMC3349367
OpenAlexW2031102024

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.