Evidence map›Paper›PMID 31933062›Full record

ArticleCellular and molecular neurobiology2020

Inhibition of USP15 Prevent Glutamate-Induced Oxidative Damage by Activating Nrf2/HO-1 Signaling Pathway in HT22 Cells.

Xiaojie Chen, Guanshui Bao, Fangfang Liu

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. The Multifaceted Roles of USP15 in Signal Transduction.International journal of molecular sciences · 2021
    Review
  10. Deubiquitinases: Modulators of Different Types of Regulated Cell Death.International journal of molecular sciences · 2021
    Review
  11. Article
  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

3 authors at 1 institution in 1 country.

Xiaojie ChenDepartment of Neurology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 201999, China.
Guanshui BaoDepartment of Neurology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 201999, China. baogs@163.com.ORCID http://orcid.org/0000-0001-5685-9322
Fangfang LiuDepartment of Neurology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 201999, China.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress has been identified as the significant mediator in epilepsy, which is a chronic disorder in central nervous system. About 30% of epilepsy patients are refractory to antiepileptic drug treatment. However, the underlying mechanism of oxidative damage in epilepsy needs further investigation. In our study, we first find that ubiquitin-specific peptidase 15 (USP15) expression was upregulated in a pentylenetetrazole (PTZ) kindled rat model of epilepsy. Silencing USP15 protected against glutamate-mediated neuronal cell death, and inhibited the high expression levels of cleaved caspase-3. Knockout of USP15 significantly reduced intracellular reactive oxygen species (ROS) levels and enhanced superoxide dismutase (SOD) activity in HT22 cells under the exposure to glutamate treatment. Furthermore, USP15 inhibition induced nuclear factor erythroid-derived 2-related factor2 (Nrf2) nuclear translocation and promoted protein expression level of heme oxygenase (HO-1). Taken together, our findings first reveal a role of USP15 in the pathogenesis of epilepsy, and silencing USP15 in vitro protects against glutamate-mediated cytotoxicity in HT22 cells. Pharmacological inhibition of USP15 may alleviate epileptic seizures via fighting against oxidative damage, providing a novel antiepileptic target.

Indexed as

Signal TransductionAnimalsCell DeathCell LineEndopeptidasesGlutamic AcidHeme Oxygenase-1Kindling, NeurologicMaleMiceNeuroprotectionNeuroprotective AgentsNF-E2-Related Factor 2Oxidative StressPentylenetetrazoleRats, Sprague-DawleyEndopeptidasesGlutamic AcidHeme Oxygenase-1Neuroprotective AgentsNF-E2-Related Factor 2Pentylenetetrazoleubiquitin-Nalpha-protein hydrolaseUbiquitin-Specific ProteasesUsp15 protein, mouseEpilepsyGlutamateNrf2/HO-1 pathwayOxidative stressUSP15

Identifiers

PMID31933062
PMCPMC11448803
OpenAlexW2999256571

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.