Evidence map›Paper›PMID 23936056›Full record

ArticlePloS one2013

Activation of store-operated calcium entry in airway smooth muscle cells: insight from a mathematical model.

Huguette Croisier, Xiahui Tan, Jose F Perez-Zoghbi, Michael J Sanderson, James Sneyd, Bindi S Brook

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Computational insights in cell physiology.Frontiers in systems biology · 2024
    Review
  3. Article
  4. Inherent differences of small airway contraction and CaFrontiers in cell and developmental biology · 2023
    Article
  5. Characterizing spontaneous CaBiophysical journal · 2022
    Article
  6. Article
  7. Article
  8. Comprehensive Simulation of CaInternational journal of molecular sciences · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Three-Dimensional Model of Sub-Plasmalemmal CaFrontiers in immunology · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Mathematical investigation of IPJournal of computational neuroscience · 2017
    Article
  18. Article
  19. Article
  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

6 authors at 4 institutions in 3 countries.

Huguette CroisierSchool of Mathematical Sciences, University of Nottingham, Nottingham, United Kingdom.
Xiahui Tan
Jose F Perez-Zoghbi
Michael J Sanderson
James Sneyd
Bindi S Brook
University of Massachusetts Chan Medical School · USUniversity of Nottingham · GBTexas Tech University Health Sciences Center · USUniversity of Auckland · NZ

Funding

A multi-scale approach to airway hyperresponsiveness: from molecule to organR01HL103405 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI BATES, JASON HT, LAUZON, ANNE-MARIE · 2010 to 2013
$3.6M
Medical Research Council G0901174NHLBI NIH HHS HL103405NHLBI NIH HHS R01 HL103405
6 · The paper itself

Abstract

Intracellular Ca(2+) dynamics of airway smooth muscle cells (ASMC) mediate ASMC contraction and proliferation, and thus play a key role in airway hyper-responsiveness (AHR) and remodelling in asthma. We evaluate the importance of store-operated Ca(2+) entry (SOCE) in these Ca(2+) dynamics by constructing a mathematical model of ASMC Ca(2+) signaling based on experimental data from lung slices. The model confirms that SOCE is elicited upon sufficient Ca(2+) depletion of the sarcoplasmic reticulum (SR), while receptor-operated [Ca(2+) entry (ROCE) is inhibited in such conditions. It also shows that SOCE can sustain agonist-induced Ca(2+) oscillations in the absence of other [Ca(2+) influx. SOCE up-regulation may thus contribute to AHR by increasing the Ca(2+) oscillation frequency that in turn regulates ASMC contraction. The model also provides an explanation for the failure of the SERCA pump blocker CPA to clamp the cytosolic Ca(2+) of ASMC in lung slices, by showing that CPA is unable to maintain the SR empty of Ca(2+). This prediction is confirmed by experimental data from mouse lung slices, and strongly suggests that CPA only partially inhibits SERCA in ASMC.

Indexed as

Models, TheoreticalAnimalsCalcium Channel BlockersCalcium ChannelsCalcium SignalingGene Expression RegulationIndolesIon TransportLungMiceMuscle ContractionMyocytes, Smooth MuscleSarcoplasmic ReticulumSarcoplasmic Reticulum Calcium-Transporting ATPasesTissue Culture TechniquesCalcium Channel BlockersCalcium Channelscyclopiazonic acidIndolesSarcoplasmic Reticulum Calcium-Transporting ATPases

Identifiers

PMID23936056
PMCPMC3723852
OpenAlexW2141955111

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.