Evidence map›Paper›PMID 27329039›Full record

ArticleMolecules and cells2016

MiR-144-3p and Its Target Gene β-Amyloid Precursor Protein Regulate 1-Methyl-4-Phenyl-1,2-3,6-Tetrahydropyridine-Induced Mitochondrial Dysfunction.

Kuo Li, Junling Zhang, Chunxue Ji, Lixuan Wang

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecules and cells, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

25 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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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

4 authors at 1 institution in 1 country.

Kuo LiNo. 2 Department of Neurology, Cangzhou Central Hospital, Cangzhou 061001, China .
Junling ZhangNo. 2 Department of Neurology, Cangzhou Central Hospital, Cangzhou 061001, China .
Chunxue JiNo. 2 Department of Neurology, Cangzhou Central Hospital, Cangzhou 061001, China .
Lixuan WangNo. 2 Department of Neurology, Cangzhou Central Hospital, Cangzhou 061001, China .
Cangzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) have been reported to be involved in many neurodegenerative diseases. The present study focused on the role of hsa-miR-144-3p in one of the neurodegenerative diseases, Parkinson's disease (PD). Our study showed a remarkable down-regulation of miR-144-3p expression in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-treated SH-SY5Y cells. MiR-144-3p was then overexpressed and silenced in human SH-SY5Y cells by miRNA-mimics and miRNA-inhibitor transfections, respectively. Furthermore, β-amyloid precursor protein (APP) was identified as a target gene of miR-144-3p via a luciferase reporter assay. We found that miR-144-3p overexpression significantly inhibited the protein expression of APP. Since mitochondrial dysfunction has been shown to be one of the major pathological events in PD, we also focused on the role of miR-144-3p and APP in regulating mitochondrial functions. Our study demonstrated that up-regulation of miR-144-3p increased expression of the key genes involved in maintaining mitochondrial function, including peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), nuclear respiratory factor 1 (NRF-1) and mitochondrial transcription factor A (TFAM). Moreover, there was also a significant increase in cellular ATP, cell viability and the relative copy number of mtDNA in the presence of miR-144-3p overexpression. In contrast, miR-144-3p silencing showed opposite effects. We also found that APP overexpression significantly decreased ATP level, cell viability, the relative copy number of mtDNA and the expression of these three genes, which reversed the effects of miR-144-3p overexpression. Taken together, these results show that miR-144-3p plays an important role in maintaining mitochondrial function, and its target gene APP is also involved in this process.

Indexed as

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAmyloid beta-Protein PrecursorCell LineCell SurvivalDNA-Binding ProteinsDNA, MitochondrialDown-RegulationGene Expression RegulationHumansMicroRNAsMitochondriaMitochondrial ProteinsModels, BiologicalNuclear Respiratory Factor 1Parkinson DiseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAmyloid beta-Protein PrecursorAPP protein, humanDNA-Binding ProteinsDNA, MitochondrialMicroRNAsMIRN144 microRNA, humanMitochondrial ProteinsNRF1 protein, humanNuclear Respiratory Factor 1Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaTFAM protein, humanTranscription Factorsamyloid precursor proteinhsa-miR-144-3pmitochondrial functionsParkinson’s disease

Identifiers

PMID27329039
PMCPMC4959019
OpenAlexW2465532580

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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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.