Evidence map›Paper›PMID 26719145›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016

Regulation of alveolar septation by microRNA-489.

Nelida Olave, Charitharth V Lal, Brian Halloran, Kusum Pandit, Alain C Cuna, Ona M Faye-Petersen, David R Kelly, Teodora Nicola, Panayiotis V Benos, Naftali Kaminski and 1 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 78 citations in OpenAlex.

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  7. FGF2 is secreted in extracellular vesicles from lung cells.American journal of physiology. Lung cellular and molecular physiology · 2024
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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

11 authors at 4 institutions in 1 country.

Nelida OlaveDepartment of Pediatrics, University of Alabama at Birmingham, Birmingham, Alabama;
Charitharth V LalDepartment of Pediatrics, University of Alabama at Birmingham, Birmingham, Alabama;
Brian HalloranDepartment of Pediatrics, University of Alabama at Birmingham, Birmingham, Alabama;
Kusum PanditDivision of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania;
Alain C CunaDepartment of Pediatrics, University of Missouri-Kansas City School of Medicine, Kansas City, Missouri;
Ona M Faye-PetersenDepartment of Pathology, University of Alabama at Birmingham, Birmingham, Alabama;
David R KellyDepartment of Pathology, University of Alabama at Birmingham, Birmingham, Alabama;
Teodora NicolaDepartment of Pediatrics, University of Alabama at Birmingham, Birmingham, Alabama;
Panayiotis V BenosDepartment of Computational & Systems Biology, University of Pittsburgh, Pittsburgh, Pennsylvania; and.
Naftali KaminskiDivision of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, Connecticut.
Namasivayam AmbalavananDepartment of Pediatrics, University of Alabama at Birmingham, Birmingham, Alabama; Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama; nambalavanan@peds.uab.edu.
University of Alabama at Birmingham · USUniversity of Pittsburgh · USUniversity of Missouri–Kansas City · USYale University · US

Funding

Alveolar DevMAPU01HL122626 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AMBALAVANAN, NAMASIVAYAM, HAGOOD, JAMES S. · 2014 to 2018
$3.7M
Molecular Phenotypes within and across disease boundaries in IPF and COPDR01HL095397 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAMINSKI, NAFTALI, SHAPIRO, STEVEN D · 2008 to 2011
$3.0M
Modeling in vivo Protein-DNA Interactions from High-Throughput Data MP1/1R01LM009657 · NLM · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BENOS, PANAGIOTIS V, KAMINSKI, NAFTALI · 2007 to 2011
$2.5M
TRANSFORMING GROWTH FACTOR - BETA MEDIATES EFFECTS OF HYPOXIA IN NEWBORN LUNGR01HL092906 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AMBALAVANAN, NAMASIVAYAM · 2008 to 2012
$1.9M
STOP BPDR01HL129907 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AMBALAVANAN, NAMASIVAYAM · 2015 to 2017
$1.1M
NHLBI NIH HHS R01 HL-092906NHLBI NIH HHS R01 HL092906NHLBI NIH HHS R01 HL-095397NHLBI NIH HHS R01 HL095397NHLBI NIH HHS R01 HL-129907NHLBI NIH HHS R01 HL129907NHLBI NIH HHS U01 HL-122626NHLBI NIH HHS U01 HL122626NLM NIH HHS R01 LM-009657NLM NIH HHS R01 LM009657
6 · The paper itself

Abstract

MicroRNAs (miRs) are small conserved RNA that regulate gene expression. Bioinformatic analysis of miRNA profiles during mouse lung development indicated a role for multiple miRNA, including miRNA-489. miR-489 increased on completion of alveolar septation [postnatal day 42 (P42)], associated with decreases in its conserved target genes insulin-like growth factor-1 (Igf1) and tenascin C (Tnc). We hypothesized that dysregulation of miR-489 and its target genes Igf1 and Tnc contribute to hyperoxia-induced abnormal lung development. C57BL/6 mice were exposed to normoxia (21%) or hyperoxia (85% O2) from P4 to P14, in combination with intranasal locked nucleic acid against miR-489 to inhibit miR-489, cytomegalovirus promoter (pCMV)-miR-489 to overexpress miR-489, or empty vector. Hyperoxia reduced miR-489 and increased Igf1 and Tnc. Locked nucleic acid against miR-489 improved lung development during hyperoxia and did not alter it during normoxia, whereas miR-489 overexpression inhibited lung development during normoxia. The 3' untranslated region in vitro reporter studies confirmed Igf1 and Tnc as targets of miR-489. While miR-489 was of epithelial origin and present in exosomes, its targets Igf1 and Tnc were produced by fibroblasts. Infants with bronchopulmonary dysplasia (BPD) had reduced lung miR-489 and increased Igf1 and Tnc compared with normal preterm or term infants. These results suggest increased miR-489 is an inhibitor of alveolar septation. During hyperoxia or BPD, reduced miR-489 and increased Igf1 and Tnc may be inadequate attempts at compensation. Further inhibition of miR-489 may permit alveolar septation to proceed. The use of specific miRNA antagonists or agonists may be a therapeutic strategy for inhibited alveolarization, such as in BPD.

Indexed as

AnimalsAnimals, NewbornBronchopulmonary DysplasiaCell ProliferationCells, CulturedDisease Models, AnimalFibroblastsHumansHyperoxiaMice, Inbred C57BLMicroRNAsPulmonary AlveoliMicroRNAsMIRN489 microRNA, humanMIRN489 microRNA, mouseinfantlung developmentmicroRNAsnewborn

Identifiers

PMID26719145
PMCPMC4773841
OpenAlexW2255350144

What OpenQuestion holds

Textmetadata
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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.