Evidence map›Paper›PMID 31334597›Full record

ArticleJournal of cellular and molecular medicine2019

LncRNA SNHG6 functions as a ceRNA to regulate neuronal cell apoptosis by modulating miR-181c-5p/BIM signalling in ischaemic stroke.

Xi'an Zhang, Zhanhui Liu, Qing Shu, Shanqi Yuan, Zhiguo Xing, Jinning Song

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
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  6. Review
  7. Transcriptomic analysis reveals molecular characterization and immune landscape of PANoptosis-related genes in atherosclerosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  8. Review
  9. Review
  10. Article
  11. Long Non-coding RNAs (lncRNAs), A New Target in Stroke.Cellular and molecular neurobiology · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Noncoding RNA crosstalk in brain health and diseases.Neurochemistry international · 2021
    Review
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.

Xi'an ZhangDepartment of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Zhanhui LiuDepartment of Neurosurgery, The Ninth Hospital of Xi'an, Xi'an, China.
Qing ShuDepartment of Pharmacy, The Ninth Hospital of Xi'an, Xi'an, China.
Shanqi YuanDepartment of Neurosurgery, The Ninth Hospital of Xi'an, Xi'an, China.
Zhiguo XingDepartment of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Jinning SongDepartment of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.ORCID 0000-0001-6338-9568
First Affiliated Hospital of Xi'an Jiaotong University · CNNinth Hospital of Nanchang · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) play important roles in the pathogenesis of brain and neurodegenerative disorders. As far as we know, the functions and potential mechanisms of small nucleolar RNA host gene 6 (SNHG6) in ischaemic stroke have not been explored. This study aimed to examine the functional role of SNHG6 in the ischaemic stroke. Middle cerebral artery occlusion (MCAO) in mice and the oxygen glucose deprivation (OGD)-induced injury in neuronal cells were applied to mimic ischaemic stroke. TTC staining, quantitative real-time PCR, cell apoptosis assay, caspase-3 activity assay, Western blot, RNA immunoprecipitation and luciferase reporter assay were performed to evaluate the function and possible mechanisms of SNHG6 in the pathogenesis of ischaemic stroke. The results show that SNHG6 expression was significantly increased both OGD-induced neuronal cells and MCAO model mice. In vitro results showed that inhibition of SNHG6 increased cell viability, inhibited cell apoptosis and caspase-3 activity in OGD-induced neuronal cells. Consistently, knockdown of SNHG6 reduced brain infarct size and improved neurological scores in the MCAO mice. Mechanistic study further revealed that SNHG6 functioned as a competing endogenous RNA (ceRNA) for miR-181c-5p, which in turn repressed its downstream target of Bcl-2 interacting mediator of cell death (BIM) and inhibiting cell apoptosis. This study revealed a novel function of SNHG6 in the modulating neuronal apoptosis in the ischaemic stroke model, and the role of SNHG6 in the regulating of neuronal apoptosis was at least partly via targeting miR-181c-5p/BIM signalling pathway.

Indexed as

AnimalsApoptosisBcl-2-Like Protein 11Brain IschemiaCaspase 3Cell SurvivalDisease Models, AnimalHumansMiceMicroRNAsNeuronsPrimary Cell CultureRNA, Long NoncodingRNA, Small InterferingStrokeBcl2l11 protein, mouseBcl-2-Like Protein 11Caspase 3MicroRNAsmirn181 microRNA, mouseRNA, Long NoncodingRNA, Small InterferingBIMcompeting endogenous RNAischaemic strokemiR-181c-5pSNHG6

Identifiers

PMID31334597
PMCPMC6714173
OpenAlexW2963033269

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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.