Evidence map›Paper›PMID 32862188›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2020

Promoting Role of Long Non-Coding RNA Small Nucleolar RNA Host Gene 15 (SNHG15) in Neuronal Injury Following Ischemic Stroke via the MicroRNA-18a/CXC Chemokine Ligand 13 (CXCL13)/ERK/MEK Axis.

Tiezhu Guo, Yueting Liu, Xinliang Ren, Wei Wang, Hanrui Liu

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.4field-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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Effect of retinoic acid on delayed encephalopathy after acute carbon monoxide poisoning: Role of the lncRNAZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Tiezhu GuoDepartment of Neurosurgery, Heji Hospital Affiliated with Changzhi Medical College, Changzhi, Shanxi, China (mainland).
Yueting LiuDepartment of Neurosurgery, The First Hospital Affiliated with Shanxi Medical University, Taiyuan, Shanxi, China (mainland).
Xinliang RenDepartment of Neurosurgery, Heji Hospital Affiliated with Changzhi Medical College, Changzhi, Shanxi, China (mainland).
Wei WangDepartment of Neurosurgery, Heji Hospital Affiliated with Changzhi Medical College, Changzhi, Shanxi, China (mainland).
Hanrui LiuDepartment of Neurology, Heji Hospital Affiliated with Changzhi Medical College, Changzhi, Shanxi, China (mainland).
Changzhi Medical College · CNShanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Long-non-coding RNA (lncRNA) SNHG15 has been reported to be an aberrantly expressed lncRNA in patients with ischemic stroke, but its role in neuronal injury following ischemic stroke remains unclear. We hypothesized that this lncRNA is associated with the pathogenesis of ischemic stroke. MATERIAL AND METHODS A mouse model of ischemic stroke was established by middle cerebral artery occlusion (MCAO). A neurogenic mouse cell line Neuro-2a (N2a) was subjected to oxygen-glucose deprivation (OGD) for in vitro experiments. Expression of SNHG15, microRNA-18a (miR-18a), and CXCL13 in mouse brain and in OGD-treated N2a cells was determined. Altered expression of SNHG15 and miR-18a was introduced to detect their roles in N2a cell viability and apoptosis. Targeting relationships between miR-18a and SNHG15 or CXCL13 were validated by luciferase assays. Cells were treated with the ERK/MEK antagonist U0126 to assess the role of the ERK/MEK signaling pathway in N2a cell growth. RESULTS SNHG15 and CXCL13 were overexpressed and miR-18a was underexpressed in MCAO-induced mice and OGD-treated N2a cells. Silencing of SNHG15 or overexpression of miR-18a promoted cell viability, while decreased cell apoptosis induced by OGD; however, subsequent disruption of the ERK/MEK signaling pathway reversed these effects. SNHG15 was found to bind to miR-18a, which could further target CXCL13. CONCLUSIONS Silencing of SNHG15 led to CXCL13 upregulation through sequestering miR-18a and the following ERK/MEK activation, thus enhancing viability while reducing apoptosis of N2a cells. SNHG15 may serve as a novel target for ischemic stroke treatment.

Indexed as

AnimalsApoptosisBrain IschemiaButadienesChemokine CXCL13Gene ExpressionMaleMiceMice, Inbred C57BLMicroRNAsMitogen-Activated Protein KinasesNitrilesProtein Kinase InhibitorsRNA, Long NoncodingRNA, Small NucleolarStrokeButadienesChemokine CXCL13Cxcl13 protein, mouseMicroRNAsMIRN18 microRNA, mouseMitogen-Activated Protein KinasesNitrilesProtein Kinase InhibitorsRNA, Long NoncodingRNA, Small NucleolarU 0126

Identifiers

PMID32862188
PMCPMC7480088
OpenAlexW3082869541

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.