Evidence map›Paper›PMID 30431059›Full record

ArticleInternational journal of molecular medicine2019

Overexpression of microRNA-183 promotes apoptosis of substantia nigra neurons via the inhibition of OSMR in a mouse model of Parkinson's disease.

Jin-Xia Gao, Yu Li, Sai-Nan Wang, Xing-Chi Chen, Lu-Lu Lin, Hui Zhang

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Jin-Xia GaoDepartment of Anesthesiology, The Second Hospital of Dalian Medical University, Dalian, Liaoning 116027, P.R. China.
Yu LiDepartment of Neurology, The Second Hospital of Dalian Medical University, Dalian, Liaoning 116027, P.R. China.
Sai-Nan WangDepartment of Neurology, The Second Hospital of Dalian Medical University, Dalian, Liaoning 116027, P.R. China.
Xing-Chi ChenDepartment of Neurology, The Second Hospital of Dalian Medical University, Dalian, Liaoning 116027, P.R. China.
Lu-Lu LinDepartment of Neurology, The Second Hospital of Dalian Medical University, Dalian, Liaoning 116027, P.R. China.
Hui ZhangDepartment of Neurology, The Second Hospital of Dalian Medical University, Dalian, Liaoning 116027, P.R. China.
Dalian Medical University · CNSecond Affiliated Hospital of Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to investigate the effect of microRNA‑183 (miR‑183) on substantia nigra neurons by targeting oncostatin M receptor (OSMR) in a mouse model of Parkinson's disease (PD). The positive expression rates of OSMR and the apoptosis of substantia nigra neurons were detected by immunohistochemistry and terminal deoxynucleotidyl transferase‑mediated dUTP‑biotin nick end‑labeling, respectively. Substantia nigra neurons in normal and PD mice were cultured in vitro. The association between miR‑183 and OSMR was verified using a dual luciferase reporter gene assay. The expression of miR‑183 and the phosphoinositide 3‑kinase‑Akt signaling pathway‑associated genes were detected by reverse transcription‑quantitative polymerase chain reaction and western blot analysis, respectively. Cell apoptosis was detected by flow cytometry. OSMR is the target gene of miR‑183. The number of OSMR‑positive cells and the apoptotic rate of substantia nigra neurons were increased in the PD group. Neurons transfected with miR‑183 mimic exhibited elevated expression levels of miR‑183, B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax) and caspase‑9 and increased apoptotic rate, and reduced expression levels of OSMR, Akt, phosphorylated (p‑)Akt, glycogen synthase kinase‑3 (GSK‑3β), p‑GSK‑3β, Bcl‑2, insulin‑like growth factor 1 (IGF‑1), mammalian target of rapamycin (mTOR) and p‑mTOR. The miR‑183 inhibitor decreased the expression levels of miR‑183, Bax and caspase‑9 and the apoptotic rate; however, increased the expression of OSMR, Akt, p‑Akt, GSK‑3β, p‑GSK‑3β, Bcl‑2, IGF‑1, mTOR and p‑mTOR. The results of the present study provide evidence that the overexpression of miR‑183 promotes the apoptosis of substantia nigra neurons by inhibiting the expression of OSMR.

Indexed as

AnimalsApoptosisBase Sequencebcl-2-Associated X ProteinBehavior, AnimalCaspase 9Disease Models, AnimalInsulin-Like Growth Factor IMaleMice, Inbred C57BLMicroRNAsNeuronsParkinson DiseaseProto-Oncogene Proteins c-aktReceptors, Oncostatin MSubstantia Nigrabcl-2-Associated X ProteinCaspase 9Insulin-Like Growth Factor IMicroRNAsMirn183 microRNA, mouseProto-Oncogene Proteins c-aktReceptors, Oncostatin MTOR Serine-Threonine Kinases

Identifiers

PMID30431059
PMCPMC6257840
OpenAlexW2899539202

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.