Evidence map›Paper›PMID 28651580›Full record

ArticleRespiratory research2017

Sex-specific lung functional changes in adult mice exposed only to second-hand smoke in utero.

Alexandra Noël, Rui Xiao, Zakia Perveen, Hasan Zaman, Viviana Le Donne, Arthur Penn

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  5. Early-life exposure to cigarette smoke primes lung function and DNA methylation changes atAmerican journal of physiology. Lung cellular and molecular physiology · 2023
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  15. Frontiers in physiology · 2021
    Article
  16. Article
  17. Article
  18. Review
  19. Pre- and postnatal exposure of mice to concentrated urban PMEnvironmental pollution (Barking, Essex : 1987) · 2018
    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 3 institutions in 2 countries.

Alexandra NoëlDepartment of Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Skip Bertman Drive, Baton Rouge, 70803, LA, USA.
Rui XiaoDepartment of Anesthesiology, Columbia University Medical Center, 622 West 168th Street, New York, 10032, NY, USA.
Zakia PerveenDepartment of Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Skip Bertman Drive, Baton Rouge, 70803, LA, USA.
Hasan ZamanDepartment of Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Skip Bertman Drive, Baton Rouge, 70803, LA, USA.
Viviana Le DonneTranslational Medicine and Comparative Pathobiology, R&D Platform Technology and Science, GlaxoSmithKline, Park Road, Ware, SG12 ODP, UK.
Arthur PennDepartment of Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Skip Bertman Drive, Baton Rouge, 70803, LA, USA. apenn1@lsu.edu.
Louisiana State University · USColumbia University Irving Medical Center · USGlaxoSmithKline (United Kingdom) · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAn increasing number of epidemiological and experimental studies have associated exposure to second-hand smoke (SHS) during pregnancy with adverse outcomes in newborns. As we have previously shown in mice, in utero exposure to SHS at critical stages of fetal development, results in altered lung responses and increased disease susceptibility upon re-exposure to irritants (SHS or ovalbumin) in adulthood. In this study, we asked whether the in utero SHS exposure alone is sufficient to alter lung structure and function in adult mice.

methodsPregnant BALB/c mice were exposed from days 6 to 19 of pregnancy to 10 mg/m

resultsIn utero SHS exposure significantly increased mean linear intercept and decreased the surface area per unit volume of the lungs in both males and females, indicating perturbation in alveolar developmental processes. Tidal volume, minute volume and inspiratory capacity were significantly decreased compared with the controls only in male mice exposed in utero to SHS, suggesting that males are more sensitive than females to an SHS insult during lung development. This also suggests that in our model, lung structure changes may be necessary but are not sufficient to impair lung function. SERPINA1A, the mouse ortholog of human α1-antitrypsin, deficiency of which is a known genetic risk factor for emphysema, was down-regulated at the protein level in the in utero SHS-exposed mice. Additionally, DNMT3A protein expression was dysregulated, indicating that DNA methylation occurred in the lungs.

conclusionsOur results indicate that in utero SHS exposure alone alters both lung function and structure well into adulthood (15 weeks) in male mice. Furthermore, lung function alterations in this model are sex-specific, with males being more susceptible to in utero SHS effects. Overall, our data suggest that in utero SHS exposure alone can predispose to adult lung diseases.

Indexed as

Sex CharacteristicsAdministration, InhalationAnimalsFemaleLungMaleMiceMice, Inbred BALB CPregnancyPrenatal Exposure Delayed EffectsTobacco Smoke PollutionTobacco Smoke PollutionIn utero exposuresLung functionLung structureSecond-hand smokeSex specificity

Identifiers

PMID28651580
PMCPMC5485620
OpenAlexW2618031952

What OpenQuestion holds

Textmetadata
LicenceCC BY
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Registered trials

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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.