Evidence map›Paper›PMID 30486773›Full record

ArticleMolecular medicine (Cambridge, Mass.)2018

Suppressed microRNA-96 inhibits iNOS expression and dopaminergic neuron apoptosis through inactivating the MAPK signaling pathway by targeting CACNG5 in mice with Parkinson's disease.

Yue Dong, Li-Li Han, Zhong-Xin Xu

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. MicroRNAs in neurodegenerative diseases: from molecular mechanisms to clinical biomarkers, detection methods and therapeutic strategies-advances and challenges.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
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  11. Neuronal microRNAs safeguard ER CaCellular and molecular life sciences : CMLS · 2022
    Article
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  15. MicroRNAs, Parkinson's Disease, and Diabetes Mellitus.International journal of molecular sciences · 2021
    Review
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  20. An Integrated Network Analysis of mRNA and Gene Expression Profiles in Parkinson's Disease.Medical science monitor : international medical journal of experimental and clinical research · 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

3 authors at 2 institutions in 1 country.

Yue DongDepartment of Neurology , China-Japan Union Hospital, Jilin University, No. 126, Xiantai Street, Erdao District, Changchun, 130012, Jilin Province, People's Republic of China.
Li-Li HanDepartment of Neurology, Cangzhou Central Hospital, Cangzhou, 061000, People's Republic of China.
Zhong-Xin XuDepartment of Neurology , China-Japan Union Hospital, Jilin University, No. 126, Xiantai Street, Erdao District, Changchun, 130012, Jilin Province, People's Republic of China. xzxxuzhongxin@126.com.
Union Hospital · CNCangzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThere have been a number of reports implicating the association of microRNAs (miRs) and the MAPK signaling pathway with the dopaminergic neuron, which is involved in the development of Parkinson's disease (PD). The present study was conducted with aims of exploring the role of miR-96 in the activation of iNOS and apoptosis of dopaminergic neuron through the MAPK signaling pathway in mice with PD.

methodsThe miR and the differentially expressed gene in PD were screened out and the relationship between them was verified. A mouse model of PD induced by MPTP and was then constructed and treated with miR-96 mimic/inhibitor and CACNG5 overexpression plasmid to extract nigral dopaminergic neuron for the purpose of detecting the effect of miR-96 on PD. The TH and iNOS positive neuronal cells, the apoptotic neuronal cells by TUNEL staining, and expression of miR-96, CACNG5, iNOS, p38MAPK, p-p38MAPK, c-Fos, Bax, and Bcl-2 in substantia nigra dopaminergic neuronal tissues were evaluated.

resultsThe results obtained from the aforementioned procedure were then verified by cell culture of the SH-SY5Y cells, followed by treatment with miR-96 mimic/inhibitor, CACNG5 overexpression plasmid and the inhibitor of the MAPK signaling pathway. CACNG5 was confirmed as a target gene of miR-96. The inhibition of miR-96 resulted in a substantial increase in nigral cells, TH positive cells and expression of CACNG5 and Bcl-2 in nigral dopaminergic neuronal tissues, and a decrease in iNOS positive cells, apoptotic neuronal cells, and expression of iNOS, p38MAPK, p-p38MAPK, c-Fos, and Bax.

conclusionThe above results implicated that the downregulation of miR-96 inhibits the activation of iNOS and apoptosis of dopaminergic neuron through the blockade of the MAPK signaling pathway by promoting CACNG5 in mice with PD.

Indexed as

AnimalsApoptosisCalcium ChannelsCell LineDisease Models, AnimalDopaminergic NeuronsDown-RegulationHumansMaleMAP Kinase Signaling SystemMice, Inbred C57BLMicroRNAsNitric Oxide Synthase Type IIParkinson DiseaseCalcium ChannelsMicroRNAsMirn96 microRNA, mouseNitric Oxide Synthase Type IINos2 protein, mouseCACNG5Dopaminergic neuronInducible nitric oxide synthaseMAPK signaling pathwayMicroRNA-96Parkinson’s disease

Identifiers

PMID30486773
PMCPMC6263543
OpenAlexW2902107783

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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.