Evidence map›Paper›PMID 31410708›Full record

ArticleNeurochemical research2019

Knockdown of TRIM32 Protects Hippocampal Neurons from Oxygen-Glucose Deprivation-Induced Injury.

Liang Wei, Jian-Shui Zhang, Sheng-Feng Ji, Hao Xu, Zhao-Hua Zhao, Li Zhang, Long Pang, Jun-Feng Zhang, Peng-Bo Yang, Hai Ma

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. The Roles of E3 Ubiquitin Ligases in Cerebral Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025
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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

10 authors at 3 institutions in 1 country.

Liang WeiDepartment of Human Anatomy & Shaanxi Key Laboratory of Brain Disorders, Xi'an Medical University, Xi'an, 710021, Shaanxi, People's Republic of China.
Jian-Shui ZhangDepartment of Human Anatomy & Histo-Embryology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, People's Republic of China.
Sheng-Feng JiDepartment of Human Anatomy & Histo-Embryology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, People's Republic of China.
Hao XuDepartment of Human Anatomy & Shaanxi Key Laboratory of Brain Disorders, Xi'an Medical University, Xi'an, 710021, Shaanxi, People's Republic of China.
Zhao-Hua ZhaoDepartment of Human Anatomy & Shaanxi Key Laboratory of Brain Disorders, Xi'an Medical University, Xi'an, 710021, Shaanxi, People's Republic of China.
Li ZhangDepartment of Human Anatomy & Shaanxi Key Laboratory of Brain Disorders, Xi'an Medical University, Xi'an, 710021, Shaanxi, People's Republic of China.
Long PangDepartment of Human Anatomy & Shaanxi Key Laboratory of Brain Disorders, Xi'an Medical University, Xi'an, 710021, Shaanxi, People's Republic of China.
Jun-Feng ZhangDepartment of Human Anatomy & Shaanxi Key Laboratory of Brain Disorders, Xi'an Medical University, Xi'an, 710021, Shaanxi, People's Republic of China. zhangjf_08@126.com.ORCID http://orcid.org/0000-0001-9461-4174
Peng-Bo YangDepartment of Human Anatomy & Histo-Embryology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, People's Republic of China. yangpengbo74@126.com.
Hai MaDepartment of Internal Neurology, Chang'an Hospital, Xi'an, 710018, Shaanxi, People's Republic of China. mahai18578@126.com.
Xi'an Medical University · CNXi'an Jiaotong University · CNChang'an University · CN

Funding

Scientific Research Program Funded by Shaanxi Provincial Education Department G201711840006Scientific Research Program Funded by Shaanxi Provincial Education Department No. G201711840002the Leading Disciplines Development Government Foundation of Shaanxi Province No. [2014]3-1001the National Natural Science Foundation of China No. 81702955the Scientific Research Program Funded by Department of Science and Technology of Shaanxi Province 2018JM7065the Scientific Research Program Funded by Department of Science and Technology of Shaanxi Province 2018KJXX-34the Scientific Research Program Funded by Department of Science and Technology of Shaanxi Province No. 2018JM7066the Shannxi Key Laboratory of Ischemic Cardiovascular Disease No. 2017ZDKF01Xi'an Medical University 2016PT06Xi'an Medical University 2017GJFY25Xi'an Medical University No. 2018XNRC07
6 · The paper itself

Abstract

Tripartite motif 32 (TRIM32) is a member of TRIM family that plays a potential role in neural regeneration. However, the biological function of TRIM32 in cerebral ischemia reperfusion injury has not been investigated. In the present study, we evaluated the expression level of TRIM32 in hippocampal neurons following oxygen-glucose deprivation/reperfusion (OGD/R). The results showed that TRIM32 expression was significantly elevated in hippocampal neurons subjected to OGD/R as compared to the neurons cultured in the normoxia condition. To further evaluate the role of TRIM32, hippocampal neurons were transfected with TRIM32 small interfering RNA (si-TRIM32) to knock down TRIM32. We found that knockdown of TRIM32 improved cell viability of OGD/R-stimulated hippocampal neurons. Generation of reactive oxygen species was decreased, while contents of superoxide dismutase and glutathione peroxidase were increased after si-TRIM32 transfection. Knockdown of TRIM32 suppressed cell apoptosis, as proved by the increased bcl-2 expression along with decreased bax expression and caspase-3 activity. We also found that TRIM32 knockdown enhanced OGD/R-induced activation of Nrf2 signaling pathway in hippocampal neurons. Furthermore, siRNA-Nrf2 was transfected to knock down Nrf2. SiRNA-Nrf2 transfection reversed the protective effects of TRIM32 knockdown on neurons. These data suggested that knockdown of TRIM32 protected hippocampal neurons from OGD/R-induced oxidative injury through activating Nrf2 signaling pathway.

Indexed as

AnimalsApoptosisFemaleGene Knockdown TechniquesGlucoseHippocampusNeuronsNeuroprotectionNF-E2-Related Factor 2Oxidative StressOxygenPregnancyRats, WistarReperfusion InjurySignal TransductionTranscription FactorsGlucoseNfe2l2 protein, ratNF-E2-Related Factor 2OxygenTranscription Factorstrim32 protein, ratTripartite Motif ProteinsUbiquitin-Protein LigasesCerebral ischemia reperfusion (I/R) injuryHippocampal neuronsNrf2 signaling pathwayOxidative stressOxygen–glucose deprivation/reperfusion (OGD/R)Tripartite totif 32 (TRIM32)

Identifiers

PMID31410708
OpenAlexW2967675702

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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.