Evidence map›Paper›PMID 27121020›Full record

ArticleRespiratory research2016

Identification of vitamin D sensitive pathways during lung development.

Ling Chen, Richard Wilson, Ellen Bennett, Graeme R Zosky

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 3 pooled it
4.4field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 3 syntheses or guidelines pooled it, 51 citations in OpenAlex.

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  18. [Protective effect of vitamin D against hyperoxia-induced bronchopulmonary dysplasia in newborn mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019
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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

4 authors at 1 institution in 1 country.

Ling ChenSchool of Medicine, Faculty of Health, University of Tasmania, Hobart, Tasmania, Australia. L.Chen@utas.edu.au.
Richard WilsonCentral Science Laboratory, University of Tasmania, Hobart, Tasmania, Australia.
Ellen BennettSchool of Medicine, Faculty of Health, University of Tasmania, Hobart, Tasmania, Australia.
Graeme R ZoskySchool of Medicine, Faculty of Health, University of Tasmania, Hobart, Tasmania, Australia.
University of Tasmania · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe have previously shown that vitamin D deficiency has a detrimental impact on lung development. In this study, we aimed to identify the mechanisms linking vitamin D with lung development using a mouse model of dietary manipulation.

methodsFemale offspring were euthanized at different time-points; embryonic day (E)14.5, E17.5 or postnatal day (P)7. Lung tissue was collected for mass spectrometry-based proteomic analysis. Label-free quantitation was used to identify the differentially expressed proteins and ELISA confirmed the expression of selected proteins. Lungs from separate groups of mice were fixed and processed for stereological assessment of lung structure.

resultsNo differences in protein expression between vitamin D deficient and replete mice were detected at E14.5 and E17.5, whereas 66 proteins were differentially expressed in P7 lungs. The expression of pulmonary surfactant-associated protein B (SP-B) and peroxiredoxin 5 (PRDX5) were reduced in P7 lungs of vitamin D deficient mice, while the production of collagen type Ι alpha 1 (COL1A1) was higher in lungs of vitamin D deficient mice. There were no differences in lung volume, parenchymal volume, volume of airspaces or surface area of airspaces between vitamin D deficient and vitamin D replete mice across three time-points.

conclusionsThe difference in protein expression during the early postnatal time-point suggests that vitamin D deficiency may induce alterations of lung structure and function in later life during alveolarization stage through impaired pulmonary surfactant production and anti-oxidative stress ability as well as enhanced collagen synthesis. These data provided a plausible mechanism linking maternal vitamin D deficiency with altered postnatal lung function.

Indexed as

AgingAnimalsCollagen Type ICollagen Type I, alpha 1 ChainFemaleGene Expression Regulation, DevelopmentalLungMaleMiceMice, Inbred BALB CPeroxiredoxinsPulmonary Surfactant-Associated Protein BSignal TransductionVitamin DCollagen Type ICollagen Type I, alpha 1 ChainPeroxiredoxinsPrdx5 protein, mousePulmonary Surfactant-Associated Protein BVitamin DCollagen type Ι alpha 1Lung developmentProteomic mass spectrometryPulmonary surfactant-associated protein BVitamin D deficiency

Identifiers

PMID27121020
PMCPMC4847230
OpenAlexW2342950709

What OpenQuestion holds

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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.