Evidence map›Paper›PMID 29324753›Full record

ArticlePloS one2018

MicroRNA signatures of endogenous Huntingtin CAG repeat expansion in mice.

Peter Langfelder, Fuying Gao, Nan Wang, David Howland, Seung Kwak, Thomas F Vogt, Jeffrey S Aaronson, Jim Rosinski, Giovanni Coppola, Steve Horvath and 1 more

Open access · goldAbstract readValidation Study
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-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

28 citing papers in PubMed, 56 citations in OpenAlex.

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  7. The Role of miR-128 in Neurodegenerative Diseases.International journal of molecular sciences · 2023
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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 2 institutions in 1 country.

Peter LangfelderDepartment of Human Genetics, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States of America.
Fuying GaoCenter for Neurobehavioral Genetics, Semel Institute for Neuroscience & Human Behavior, University of California Los Angeles (UCLA), Los Angeles, CA, United States of America.
Nan WangCenter for Neurobehavioral Genetics, Semel Institute for Neuroscience & Human Behavior, University of California Los Angeles (UCLA), Los Angeles, CA, United States of America.
David HowlandCHDI Foundation/CHDI Management Inc., Princeton, NJ, United States of America.
Seung KwakCHDI Foundation/CHDI Management Inc., Princeton, NJ, United States of America.
Thomas F VogtCHDI Foundation/CHDI Management Inc., Princeton, NJ, United States of America.
Jeffrey S AaronsonCHDI Foundation/CHDI Management Inc., Princeton, NJ, United States of America.
Jim RosinskiCHDI Foundation/CHDI Management Inc., Princeton, NJ, United States of America.
Giovanni CoppolaCenter for Neurobehavioral Genetics, Semel Institute for Neuroscience & Human Behavior, University of California Los Angeles (UCLA), Los Angeles, CA, United States of America.
Steve HorvathDepartment of Human Genetics, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States of America.
X William YangCenter for Neurobehavioral Genetics, Semel Institute for Neuroscience & Human Behavior, University of California Los Angeles (UCLA), Los Angeles, CA, United States of America.ORCID 0000-0003-3705-7935
University of California, Los Angeles · USCHDI Foundation · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In Huntington's disease (HD) patients and in model organisms, messenger RNA transcriptome has been extensively studied; in contrast, comparatively little is known about expression and potential role of microRNAs. Using RNA-sequencing, we have quantified microRNA expression in four brain regions and liver, at three different ages, from an allelic series of HD model mice with increasing CAG length in the endogenous Huntingtin gene. Our analyses reveal CAG length-dependent microRNA expression changes in brain, with 159 microRNAs selectively altered in striatum, 102 in cerebellum, 51 in hippocampus, and 45 in cortex. In contrast, a progressive CAG length-dependent microRNA dysregulation was not observed in liver. We further identify microRNAs whose transcriptomic response to CAG length expansion differs significantly among the brain regions and validate our findings in data from a second, independent cohort of mice. Using existing mRNA expression data from the same animals, we assess the possible relationships between microRNA and mRNA expression and highlight candidate microRNAs that are negatively correlated with, and whose predicted targets are enriched in, CAG-length dependent mRNA modules. Several of our top microRNAs (Mir212/Mir132, Mir218, Mir128 and others) have been previously associated with aspects of neuronal development and survival. This study provides an extensive resource for CAG length-dependent changes in microRNA expression in disease-vulnerable and -resistant brain regions in HD mice, and provides new insights for further investigation of microRNAs in HD pathogenesis and therapeutics.

Indexed as

Trinucleotide RepeatsAnimalsBrainHumansHuntingtin ProteinHuntington DiseaseMiceMicroRNAsTranscriptomeHTT protein, humanHuntingtin ProteinMicroRNAs

Identifiers

PMID29324753
PMCPMC5764268
OpenAlexW2784189030

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.