Evidence map›Paper›PMID 30977043›Full record

ArticleNeuroscience bulletin2019

MicroRNA-365 Knockdown Prevents Ischemic Neuronal Injury by Activating Oxidation Resistance 1-Mediated Antioxidant Signals.

Jia-Lin Mo, Zhi-Guang Pan, Xiao Chen, Yu Lei, Ling-Ling Lv, Cheng Qian, Feng-Yan Sun

Open access · greenAbstract read
In one paragraph

Article in Neuroscience bulletin, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. MicroRNA Profiles in Critically Ill Patients.Current medicinal chemistry · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Neurovascular Unit: A critical role in ischemic stroke.CNS neuroscience & therapeutics · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. 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 3 institutions in 1 country.

Jia-Lin MoDepartment of Neurobiology and Institute for Basic Research on Aging and Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
Zhi-Guang PanDepartment of Neurosurgery, National Clinical Research Center for Aging and Medicine, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Xiao ChenDepartment of Neurobiology and Institute for Basic Research on Aging and Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
Yu LeiDepartment of Neurobiology and Institute for Basic Research on Aging and Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
Ling-Ling LvDepartment of Neurobiology and Institute for Basic Research on Aging and Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
Cheng QianDepartment of Neurobiology and Institute for Basic Research on Aging and Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
Feng-Yan SunDepartment of Neurobiology and Institute for Basic Research on Aging and Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China. fysun@shmu.edu.cn.
Fudan University · CNHuashan Hospital · CNState Key Laboratory of Medical Neurobiology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA-365 (miR-365) is upregulated in the ischemic brain and is involved in oxidative damage in the diabetic rat. However, it is unclear whether miR-365 regulates oxidative stress (OS)-mediated neuronal damage after ischemia. Here, we used a transient middle cerebral artery occlusion model in rats and the hydrogen peroxide-induced OS model in primary cultured neurons to assess the roles of miR-365 in neuronal damage. We found that miR-365 exacerbated ischemic brain injury and OS-induced neuronal damage and was associated with a reduced expression of OXR1 (Oxidation Resistance 1). In contrast, miR-365 antagomir alleviated both the brain injury and OXR1 reduction. Luciferase assays indicated that miR-365 inhibited OXR1 expression by directly targeting the 3'-untranslated region of Oxr1. Furthermore, knockdown of OXR1 abolished the neuroprotective and antioxidant effects of the miR-365 antagomir. Our results suggest that miR-365 upregulation increases oxidative injury by inhibiting OXR1 expression, while its downregulation protects neurons from oxidative death by enhancing OXR1-mediated antioxidant signals.

Indexed as

AnimalsAntioxidantsBrain IschemiaCells, CulturedGene Knockdown TechniquesHydrogen PeroxideMaleMicroRNAsMitochondrial ProteinsNeuroprotectionOxidative StressRatsRats, Sprague-DawleyAntioxidantsHydrogen PeroxideMicroRNAsMIRN365 microRNA, ratMitochondrial ProteinsOxr1 protein, mouseIschemic strokeMicroRNANeuronal damageNeuroprotectionOxidative stress

Identifiers

PMID30977043
PMCPMC6754487
OpenAlexW2940018154

What OpenQuestion holds

Textmetadata
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.