Evidence map›Paper›PMID 27080144›Full record

ArticleScientific reports2016

MiR-299-5p regulates apoptosis through autophagy in neurons and ameliorates cognitive capacity in APPswe/PS1dE9 mice.

Yueqi Zhang, Chengeng Liu, Jinling Wang, Qiliang Li, Hong Ping, Shichao Gao, Peichang Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
6.0field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 73 citations in OpenAlex.

  1. Exploring dysregulated miRNAs in cryptorchidism: a systematic review.The Journal of international medical research · 2021
    Pooled it
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  15. The Potential Role of miRNA-Regulated Autophagy in Alzheimer's Disease.International journal of molecular sciences · 2022
    Review
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  17. Article
  18. Autophagy and apoptosis cascade: which is more prominent in neuronal death?Cellular and molecular life sciences : CMLS · 2021
    Review
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  20. Article
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

7 authors at 1 institution in 1 country.

Yueqi ZhangClinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China.
Chengeng LiuClinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China.
Jinling WangClinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China.
Qiliang LiDepartment of Medical Laboratory of Beijing Children's Hospital, Capital Medical University, Beijing 100053, P.R. China.
Hong PingClinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China.
Shichao GaoClinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China.
Peichang WangClinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China.
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormalities of autophagy can result in neurodegenerative disorders such as Alzheimer's disease (AD). Nevertheless, the regulatory mechanisms of autophagy in AD are not well understood. Here, we describe our findings that microRNA (miR)-299-5p functions as an autophagy inhibitor by suppressing Atg5 and antagonizing caspase-dependent apoptosis. We observed decreased levels of miR-299-5p both in primary neurons under conditions of starvation and in hippocampi of APPswe/PS1dE9 mice. Additionally, low levels of miR-299-5p were observed in cerebrospinal fluid of AD patients. MiR-299-5p treatment resulted in attenuation of Atg5 and autophagy in primary neurons from APPswe/PS1dE9 mice, N2a cells and SH-SY5Y cells, whereas antagomiR-299-5p enhanced autophagy. Atg5 was verified as a direct target of miR-299-5p by dual luciferase reporter assays. Furthermore, transfection of miR-299-5p into primary hippocampal neurons caused the attenuation of caspase-mediated apoptosis, which was reversed upon starvation-induced autophagy. Inhibition of autophagy by shRNA knockdown of LC3β reduced apoptotic neuron death induced by antagomiR-299-5p. Injection of agomiR-299-5p into the cerebral ventricles of AD mice inhibited both autophagy and apoptosis and also improved the cognitive performance of mice. Overall, our results suggest that miR-299-5p modulates neuron survival programs by regulating autophagy. Thus, miR-299-5p serves as a potential neuroprotective factor in AD.

Indexed as

Amyloid beta-Protein PrecursorAnimalsApoptosisAutophagyCell LineCognition DisordersHippocampusHumansMiceMice, TransgenicMicroRNAsNeuronsPresenilin-1Amyloid beta-Protein PrecursorMicroRNAsMIRN299 microRNA, mousePresenilin-1

Identifiers

PMID27080144
PMCPMC4832239
OpenAlexW2341787609

What OpenQuestion holds

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LicenceCC BY
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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.