Evidence map›Paper›PMID 26376480›Full record

ArticlePloS one2015

The Potential Regulatory Mechanisms of miR-196a in Huntington's Disease through Bioinformatic Analyses.

Mu-Hui Fu, Chia-Ling Li, Hsiu-Lien Lin, Shaw-Jeng Tsai, Yen-Yu Lai, Yu-Fan Chang, Pei-Hsun Cheng, Chuan-Mu Chen, Shang-Hsun Yang

Open access · goldAbstract readComparative Study
In one paragraph

Article in PloS one, 2015. 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
0.9field-weighted citation impact, top 25% 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, 37 citations in OpenAlex.

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  15. Circulating RNAs as Potential Biomarkers in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2020
    Review
  16. Exploration of targets regulated by miR-125b in porcine adipocytes.In vitro cellular & developmental biology. Animal · 2020
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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

9 authors at 2 institutions in 1 country.

Mu-Hui FuInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan; Department of Neurology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Chia-Ling LiInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
Hsiu-Lien LinInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan; Division of Breeding and Genetics, Livestock Research Institute, Council of Agriculture, Tainan 71246, Taiwan.
Shaw-Jeng TsaiInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan; Department of Physiology, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
Yen-Yu LaiDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
Yu-Fan ChangDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
Pei-Hsun ChengDepartment of Physiology, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
Chuan-Mu ChenDepartment of Life Sciences, Agricultural Biotechnology Center, National Chung Hsing University, Taichung 40227, Taiwan.
Shang-Hsun YangInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan; Department of Physiology, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
National Cheng Kung University · TWNational Chung Hsing University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High throughput screening is a powerful tool to identify the potential candidate molecules involved during disease progression. However, analysis of complicated data is one of the most challenging steps on the way to obtaining useful results from this approach. Previously, we showed that a specific miRNA, miR-196a, could ameliorate the pathological phenotypes of Huntington's disease (HD) in different models, and performed high throughput screening by using the striatum of transgenic mice. In this study, we further tried to identify the potential regulatory mechanisms using different bioinformatic tools, including Database for Annotation, Visualization and Integrated Discovery (DAVID), Molecular Signatures Database (MSigDB), TargetScan and MetaCore. The results showed that miR-196a dominantly altered "ABC transporters", "RIG-I-like receptor signaling pathway", immune system", "adaptive immune system","tissue remodeling and wound repair" and "cytoskeleton remodeling". In addition, miR-196a also changed the expression of several well-defined pathways of HD, such as apoptosis and cell adhesion. Since these analyses showed the regulatory pathways are highly related to the modification of the cytoskeleton, we further confirmed that miR-196a could enhance the neurite outgrowth in neuroblastoma cells, suggesting miR-196a might provide beneficial functions through the alteration of cytoskeleton structures. Since impairment of the cytoskeleton has been reported in several neuronal diseases, this study will provide not only the potential working mechanisms of miR-196a but also insights for therapeutic strategies for use with different neuronal diseases.

Indexed as

Gene Expression RegulationAnimalsBiomarkersComputational BiologyCorpus StriatumDisease Models, AnimalGene Expression ProfilingHuntington DiseaseMiceMice, TransgenicMicroRNAsNeuritesNeuroblastomaPhenotypeBiomarkersMicroRNAsMIRN196 microRNA, human

Identifiers

PMID26376480
PMCPMC4574104
OpenAlexW2208872982

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.