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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 ZhangEmail author
  • Peng-bo YangEmail author
  • Hai MaEmail author
Original Paper
  • 35 Downloads

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.

Keywords

Tripartite totif 32 (TRIM32) Cerebral ischemia reperfusion (I/R) injury Hippocampal neurons Oxygen–glucose deprivation/reperfusion (OGD/R) Oxidative stress Nrf2 signaling pathway 

Notes

Acknowledgement

This work was supported by the National Natural Science Foundation of China (No. 81702955), the Scientific Research Program Funded by Department of Science and Technology of Shaanxi Province (Nos. 2018JM7066, 2018JM7065, 2018KJXX-34, 2019JZ-38), Scientific Research Program Funded by Shaanxi Provincial Education Department (Nos. G201711840002, G201711840006), the Leading Disciplines Development Government Foundation of Shaanxi Province (No.[2014]3-1001), grant from the Shannxi Key Laboratory of Ischemic Cardiovascular Disease (No. 2017ZDKF01), supporting Program Funded by Xi’an Medical University (Nos. 2018XNRC07, 2018GJFY02, 2017GJFY25, 2016PT06).

Compliance with Ethical Standards

Conflicts of interest

The authors have no competing interests to disclose.

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© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  1. 1.Department of Human Anatomy & Shaanxi Key Laboratory of Brain DisordersXi’an Medical UniversityXi’anPeople’s Republic of China
  2. 2.Department of Human Anatomy & Histo-Embryology, School of Basic Medical SciencesXi’an Jiaotong University Health Science CenterXi’anPeople’s Republic of China
  3. 3.Department of Internal NeurologyChang’an HospitalXi’anPeople’s Republic of China
  4. 4.Shaanxi Key Laboratory of Ischemic Cardiovascular Disease, Institute of Basic and Translational MedicineXi’an Medical UniversityXi’anPeople’s Republic of China

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