Evidence map›Paper›PMID 26891231›Full record

ArticlePloS one2016

MiR-449a Affects Epithelial Proliferation during the Pseudoglandular and Canalicular Phases of Avian and Mammal Lung Development.

Ethan L Sanford, Kwong W Choy, Patricia K Donahoe, Adam A Tracy, Regis Hila, Maria Loscertales, Mauro Longoni

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.5field-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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. miRNAs in Lung Development and Diseases.International journal of molecular sciences · 2020
    Review
  10. Heterochronic regulation of lung developmentFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. 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

7 authors at 4 institutions in 2 countries.

Ethan L SanfordPediatric Surgical Research Laboratories, Massachusetts General Hospital, Boston, MA, United States of America.
Kwong W ChoyDepartment of Obstetrics & Gynaecology, The Chinese University of Hong Kong, Hong Kong, China.
Patricia K DonahoeDepartment of Surgery, Harvard Medical School, Boston, MA, United States of America.
Adam A TracyDepartment of Surgery, Harvard Medical School, Boston, MA, United States of America.
Regis HilaPediatric Surgical Research Laboratories, Massachusetts General Hospital, Boston, MA, United States of America.
Maria LoscertalesPediatric Surgical Research Laboratories, Massachusetts General Hospital, Boston, MA, United States of America.
Mauro LongoniPediatric Surgical Research Laboratories, Massachusetts General Hospital, Boston, MA, United States of America.
Harvard University · USMassachusetts General Hospital · USBroad Institute · USChinese University of Hong Kong · CN

Funding

THE DROSOPHILA GENETICS AND RNAI CORE (THE FLY CORE)P01HD068250 · NICHD · MASSACHUSETTS GENERAL HOSPITAL · PI CHUNG, WENDY K, DONAHOE, PATRICIA K · 2011 to 2022
$17.1M
NICHD NIH HHS P01 HD068250NICHD NIH HHS P01 HD068250-03
6 · The paper itself

Abstract

Congenital diaphragmatic hernia is associated with pulmonary hypoplasia and respiratory distress, which result in high mortality and morbidity. Although several transgenic mouse models of lung hypoplasia exist, the role of miRNAs in this phenotype is incompletely characterized. In this study, we assessed microRNA expression levels during the pseudoglandular to canalicular phase transition of normal human fetal lung development. At this critical time, when the distal respiratory portion of the airways begins to form, microarray analysis showed that the most significantly differentially expressed miRNA was miR-449a. Prediction algorithms determined that N-myc is a target of miR-449a and identified the likely miR-449a:N-myc binding sites, confirmed by luciferase assays and targeted mutagenesis. Functional ex vivo knock-down in organ cultures of murine embryonic lungs, as well as in ovo overexpression in avian embryonic lungs, suggested a role for miR-449a in distal epithelial proliferation. Finally, miR-449a expression was found to be abnormal in rare pulmonary specimens of human fetuses with Congenital Diaphragmatic Hernia in the pseudoglandular or canalicular phase. This study confirms the conserved role of miR-449a for proper pulmonary organogenesis, supporting the delicate balance between expansion of progenitor cells and their terminal differentiation, and proposes the potential involvement of this miRNA in human pulmonary hypoplasia.

Indexed as

3' Untranslated RegionsAnimalsBase SequenceBinding SitesCell DifferentiationCell ProliferationChickensGene Expression Regulation, DevelopmentalHumansLungMiceMicroRNAsOncogene ProteinsOrganogenesisRNA InterferenceRNA, Messenger3' Untranslated RegionsMicroRNAsOncogene ProteinsRNA, Messenger

Identifiers

PMID26891231
PMCPMC4758652
OpenAlexW2285549980

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.