Evidence map›Paper›PMID 28383034›Full record

ArticleScientific reports2017

Pulmonary microRNA profiles identify involvement of Creb1 and Sec14l3 in bronchial epithelial changes in allergic asthma.

Sabine Bartel, Nikola Schulz, Francesca Alessandrini, Andrea C Schamberger, Philipp Pagel, Fabian J Theis, Katrin Milger, Elfriede Noessner, Stephen M Stick, Anthony Kicic and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. miR-144/451: A Regulatory Role in Inflammation.Current molecular medicine · 2025
    Review
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  10. Deletion of theAnnals of translational medicine · 2022
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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

13 authors at 6 institutions in 3 countries.

Sabine BartelEarly origins of chronic lung disease, Priority Area Asthma &Allergy, Research Center Borstel, Leibniz-Center for Medicine and Biosciences, Airway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany.
Nikola SchulzComprehensive Pneumology Center (CPC-M), Institute of Lung Biology and Disease, Helmholtz Zentrum München and University Hospital of the Ludwig Maximilians University (LMU), Member of the German Center for Lung Research (DZL), Munich, Germany.
Francesca AlessandriniCenter of Allergy and Environment (ZAUM), Technische Universität and Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Munich, Germany.
Andrea C SchambergerComprehensive Pneumology Center (CPC-M), Institute of Lung Biology and Disease, Helmholtz Zentrum München and University Hospital of the Ludwig Maximilians University (LMU), Member of the German Center for Lung Research (DZL), Munich, Germany.
Philipp PagelNumares Health, Regensburg, Germany.
Fabian J TheisInstitute of Computational Biology, Helmholtz Zentrum München and Department of Mathematics, Technische Universität München, Munich, Germany.
Katrin MilgerComprehensive Pneumology Center (CPC-M), Institute of Lung Biology and Disease, Helmholtz Zentrum München and University Hospital of the Ludwig Maximilians University (LMU), Member of the German Center for Lung Research (DZL), Munich, Germany.
Elfriede NoessnerInstitute of Molecular Immunology, Helmholtz Zentrum München, Munich, Germany.
Stephen M StickTelethon Kids Institute, Centre for Health Research, The University of Western Australia, Nedlands, 6009, Western Australia, Australia.
Anthony KicicTelethon Kids Institute, Centre for Health Research, The University of Western Australia, Nedlands, 6009, Western Australia, Australia.
Oliver EickelbergComprehensive Pneumology Center (CPC-M), Institute of Lung Biology and Disease, Helmholtz Zentrum München and University Hospital of the Ludwig Maximilians University (LMU), Member of the German Center for Lung Research (DZL), Munich, Germany.
Robert J FreishtatDivision of Emergency Medicine, Children's National Medical Center, Washington DC, USA.
Susanne Krauss-EtschmannEarly origins of chronic lung disease, Priority Area Asthma &Allergy, Research Center Borstel, Leibniz-Center for Medicine and Biosciences, Airway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany.
Helmholtz Zentrum München · DEChildren's National · USGerman Center for Lung Research · DELudwig-Maximilians-Universität München · DEPrincess Margaret Hospital for Children · AUThe University of Western Australia · AU

Funding

Vitamin D, Steroids, and Asthma in African American YouthR01MD007075 · NIMHD · CHILDREN'S RESEARCH INSTITUTE · PI FREISHTAT, ROBERT J · 2012 to 2016
$2.2M
NIMHD NIH HHS R01 MD007075
6 · The paper itself

Abstract

Asthma is highly prevalent, but current therapies cannot influence the chronic course of the disease. It is thus important to understand underlying early molecular events. In this study, we aimed to use microRNAs (miRNAs) - which are critical regulators of signaling cascades - to identify so far uncharacterized asthma pathogenesis pathways. Therefore, deregulation of miRNAs was assessed in whole lungs from mice with ovalbumin (OVA)-induced allergic airway inflammation (AAI). In silico predicted target genes were confirmed in reporter assays and in house-dust-mite (HDM) induced AAI and primary human bronchial epithelial cells (NHBE) cultured at the air-liquid interface. We identified and validated the transcription factor cAMP-responsive element binding protein (Creb1) and its transcriptional co-activators (Crtc1-3) as targets of miR-17, miR-144, and miR-21. Sec14-like 3 (Sec14l3) - a putative target of Creb1 - was down-regulated in both asthma models and in NHBE cells upon IL13 treatment, while it's expression correlated with ciliated cell development and decreased along with increasing goblet cell metaplasia. Finally, we propose that Creb1/Crtc1-3 and Sec14l3 could be important for early responses of the bronchial epithelium to Th2-stimuli. This study shows that miRNA profiles can be used to identify novel targets that would be overlooked in mRNA based strategies.

Indexed as

AnimalsAsthmaBronchiCarrier ProteinsCell DifferentiationCells, CulturedCyclic AMP Response Element-Binding ProteinDown-RegulationEpithelial CellsFemaleForkhead Transcription FactorsGene Expression ProfilingGoblet CellsHumansHypersensitivityInflammationCarrier ProteinsCREB1 protein, humanCrtc1 protein, mouseCyclic AMP Response Element-Binding ProteinForkhead Transcription FactorsFOXJ1 protein, humanInterleukin-13MicroRNAsSEC14L3 protein, humanSec14l3 protein, mouseTranscription Factors

Identifiers

PMID28383034
PMCPMC5382551
OpenAlexW2605219304

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.