Evidence map›Paper›PMID 24218621›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Establishment of smooth muscle and cartilage juxtaposition in the developing mouse upper airways.

Elizabeth A Hines, Mary-Kayt N Jones, Jamie M Verheyden, Julie F Harvey, Xin Sun

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

43 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
  7. Article
  8. Observational
  9. Article
  10. Article
  11. BMP4 and Wnt signaling interact to promote mouse tracheal mesenchyme morphogenesis.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  12. Article
  13. Review
  14. Article
  15. Tracheal Ring Formation.Frontiers in cell and developmental biology · 2022
    Review
  16. Molecular crosstalk in tracheal development and its recurrence in adult tissue regeneration.Developmental dynamics : an official publication of the American Association of Anatomists · 2021
    Review
  17. Article
  18. Article
  19. 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.

Elizabeth A HinesLaboratory of Genetics, University of Wisconsin, Madison, WI 53706.
Mary-Kayt N Jones
Jamie M Verheyden
Julie F Harvey
Xin Sun
University of Wisconsin–Madison · US

Funding

FGF Signaling in Lung Maturation and Response to InjuryR01HL113870 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI SUN, XIN · 2012 to 2016
$2.1M
Cartilage and Smooth Muscle in Airway Tone and MicroenvironmentR01HL119946 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI SUN, XIN · 2014 to 2017
$2.1M
NHLBI NIH HHS HL113870NHLBI NIH HHS R01 HL113870NHLBI NIH HHS R01 HL119946
6 · The paper itself

Abstract

In the trachea and bronchi of the mouse, airway smooth muscle (SM) and cartilage are localized to complementary domains surrounding the airway epithelium. Proper juxtaposition of these tissues ensures a balance of elasticity and rigidity that is critical for effective air passage. It is unknown how this tissue complementation is established during development. Here we dissect the developmental relationship between these tissues by genetically disrupting SM formation (through Srf inactivation) or cartilage formation (through Sox9 inactivation) and assessing the impact on the remaining lineage. We found that, in the trachea and main bronchi, loss of SM or cartilage resulted in an increase in cell number of the remaining lineage, namely the cartilage or SM, respectively. However, only in the main bronchi, but not in the trachea, did the loss of SM or cartilage lead to a circumferential expansion of the remaining cartilage or SM domain, respectively. In addition to SM defects, cartilage-deficient tracheas displayed epithelial phenotypes, including decreased basal cell number, precocious club cell differentiation, and increased secretoglobin expression. These findings together delineate the mechanisms through which a cell-autonomous disruption of one structural tissue can have widespread consequences on upper airway function.

Indexed as

AnimalsBronchiCartilageFluorescent Antibody TechniqueIn Situ HybridizationLungMiceMorphogenesisMuscle, SmoothReal-Time Polymerase Chain ReactionSOX9 Transcription FactorTracheaTracheomalaciaSox9 protein, mouseSOX9 Transcription Factorairway developmenttracheomalacia

Identifiers

PMID24218621
PMCPMC3845103
OpenAlexW2144777356

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.