Evidence map›Paper›PMID 27005422›Full record

ArticleHuman molecular genetics2016

Cell-type-specific miR-431 dysregulation in a motor neuron model of spinal muscular atrophy.

Mary H Wertz, Kellen Winden, Pierre Neveu, Shi-Yan Ng, Ebru Ercan, Mustafa Sahin

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 42 citations in OpenAlex.

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  15. Mechanism of microRNA-431-5p-Archives of medical science : AMS · 2019
    Article
  16. Hyperexcitability precedes motoneuron loss in theJournal of neurophysiology · 2019
    Article
  17. Article
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  20. [Continuous expression of miR-431 during lung development in Sprague-Dawley rats].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2019
    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 4 institutions in 3 countries.

Mary H WertzDepartment of Neurology, The F. M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Kellen WindenDepartment of Neurology, The F. M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Pierre NeveuCell Biology and Biophysics Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany.
Shi-Yan NgDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA Neurotherapeutics Laboratory, Institute of Molecular and Cell Biology, A*STAR, Singapore 138673, Singapore.
Ebru ErcanDepartment of Neurology, The F. M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Mustafa SahinDepartment of Neurology, The F. M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA mustafa.sahin@childrens.harvard.edu.
Boston Children's Hospital · USHarvard University · USEuropean Molecular Biology Laboratory · DEInstitute of Molecular and Cell Biology · SG

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
Mouse Neurodevelopmental Behavior CoreU54HD090255 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI SAHIN, MUSTAFA · 2016 to 2020
$5.2M
NICHD NIH HHS P30 HD018655NICHD NIH HHS U54 HD090255
6 · The paper itself

Abstract

Spinal muscular atrophy (SMA) is an autosomal-recessive pediatric neurodegenerative disease characterized by selective loss of spinal motor neurons. It is caused by mutation in the survival of motor neuron 1, SMN1, gene and leads to loss of function of the full-length SMN protein. microRNAs (miRNAs) are small RNAs that are involved in post-transcriptional regulation of gene expression. Prior studies have implicated miRNAs in the pathogenesis of motor neuron disease. We hypothesized that motor neuron-specific miRNA expression changes are involved in their selective vulnerability in SMA. Therefore, we sought to determine the effect of SMN loss on miRNAs and their target mRNAs in spinal motor neurons. We used microarray and RNAseq to profile both miRNA and mRNA expression in primary spinal motor neuron cultures after acute SMN knockdown. By integrating the miRNA:mRNA profiles, a number of dysregulated miRNAs were identified with enrichment in differentially expressed putative mRNA targets. miR-431 expression was highly increased, and a number of its putative mRNA targets were significantly downregulated in motor neurons after SMN loss. Further, we found that miR-431 regulates motor neuron neurite length by targeting several molecules previously identified to play a role in motor neuron axon outgrowth, including chondrolectin. Together, our findings indicate that cell-type-specific dysregulation of miR-431 plays a role in the SMA motor neuron phenotype.

Indexed as

AnimalsDisease Models, AnimalGene Expression RegulationHigh-Throughput Nucleotide SequencingHumansMiceMice, KnockoutMicroarray AnalysisMicroRNAsMotor NeuronsMuscular Atrophy, SpinalNeuritesSurvival of Motor Neuron 1 ProteinMicroRNAsMIRN431 microRNA, mouseSmn1 protein, mouseSurvival of Motor Neuron 1 Protein

Identifiers

PMID27005422
PMCPMC6281359
OpenAlexW2307662723

What OpenQuestion holds

Textmetadata
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.