Evidence map›Paper›PMID 24669775›Full record

ArticleAmerican journal of respiratory cell and molecular biology2014

Mitotic asynchrony induces transforming growth factor-β1 secretion from airway epithelium.

Sarah E Alcala, Angela S Benton, Alan M Watson, Suraiya Kureshi, Erica M K Reeves, Jesse Damsker, Zuyi Wang, Kanneboyina Nagaraju, Julia Anderson, Aaron M Williams and 5 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 30% 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, 12 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Conditional reprogramming of pediatric airway epithelial cells: A new human model to investigate early-life respiratory disorders.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2017
    Article
  6. Article
  7. A Heterotopic Xenograft Model of Human Airways for Investigating Fibrosis in Asthma.American journal of respiratory cell and molecular biology · 2017
    Article
  8. Article
  9. Article
  10. Asthma.Nature reviews. Disease primers · 2015
    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

15 authors at 2 institutions in 1 country.

Sarah E Alcala1 Division of Emergency Medicine, and.
Angela S Benton
Alan M Watson
Suraiya Kureshi
Erica M K Reeves
Jesse Damsker
Zuyi Wang
Kanneboyina Nagaraju
Julia Anderson
Aaron M Williams
Amber J Y Lee
Kathleen Hayes
Mary C Rose
Eric P Hoffman
Robert J Freishtat
Children's National · USReveraGen BioPharma (United States) · US

Funding

Clinical and Translational Science Institute at Children's NationalUL1TR000075 · NCATS · CHILDREN'S RESEARCH INSTITUTE · PI GUAY-WOODFORD, LISA MARIE · 2012 to 2015
$13.7M
Anti-inflammatory and Mitotic Properties of Non-hormonal Steroids in Lung EpithelR41HL104939 · NHLBI · REVERAGEN BIOPHARMA, INC. · PI REEVES, ERICA · 2010 to 2010
$375k
NCATS NIH HHS UL1 TR000075NCATS NIH HHS UL1TR000075NHLBI NIH HHS R41 HL104939NHLBI NIH HHS R41HL104939
6 · The paper itself

Abstract

We recently proposed that mitotic asynchrony in repairing tissue may underlie chronic inflammation and fibrosis, where immune cell infiltration is secondary to proinflammatory cross-talk among asynchronously repairing adjacent tissues. Building on our previous finding that mitotic asynchrony is associated with proinflammatory/fibrotic cytokine secretion (e.g., transforming growth factor [TGF]-β1), here we provide evidence supporting cause-and-effect. Under normal conditions, primary airway epithelial basal cell populations undergo mitosis synchronously and do not secrete proinflammatory or profibrotic cytokines. However, when pairs of nonasthmatic cultures were mitotically synchronized at 12 hours off-set and then combined, the mixed cell populations secreted elevated levels of TGF-β1. This shows that mitotic asynchrony is not only associated with but is also causative of TGF-β1 secretion. The secreted cytokines and other mediators from asthmatic cells were not the cause of asynchronous regeneration; synchronously mitotic nonasthmatic epithelia exposed to conditioned media from asthmatic cells did not show changes in mitotic synchrony. We also tested if resynchronization of regenerating asthmatic airway epithelia reduces TGF-β1 secretion and found that pulse-dosed dexamethasone, simvastatin, and aphidicolin were all effective. We therefore propose a new model for chronic inflammatory and fibrotic conditions where an underlying factor is mitotic asynchrony.

Indexed as

MitosisAphidicolinAsthmaBronchiCells, CulturedCulture Media, ConditionedDexamethasoneEpithelial CellsEpitheliumFibrosisHumansInflammationRespiratory MucosaSimvastatinTime FactorsTransforming Growth Factor beta1AphidicolinCulture Media, ConditionedDexamethasoneSimvastatinTGFB1 protein, humanTransforming Growth Factor beta1asthmafibrosismitosistransforming growth factor-β1

Identifiers

PMID24669775
PMCPMC4189490
OpenAlexW2125991960

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.