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Knocking out Selenium Binding Protein 1 Induces Depressive-Like Behavior in Mice

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Abstract

Selenium binding protein 1 (SELENBP1) is involved in neurologic disorders, such as multiple sclerosis, spinal cord injury, Parkinson’s disease, epilepsy, and schizophrenia. However, the role of SELENBP1 in the neurogenesis of depression, which is a neurologic disorder, and the underlying mechanisms of oxidative stress and inflammation in depression remain unknown. In this study, we evaluated the changes in the expression levels of SELENBP1 in the hippocampus of a mouse model of depression and in the serum of human patients with depression using the Gene Expression Omnibus database. These changes were validated using blood samples from human patients with depression and mouse models with chronic unpredictable mild stress (CUMS)-induced depressive-like behavior. We also investigated the effects of SELENBP1 knockout (KO) on inflammation, oxidative stress, and hippocampal neurogenesis in mice with CUMS-induced depression. Our results revealed that SELENBP1 levels was decreased in the blood of human patients with depression and in the hippocampus of mice with CUMS-induced depression. SELENBP1 KO increased CUMS-induced depressive behavior in mice and caused dysregulation of inflammatory cytokines and oxidative stress. This led to a decrease in the numbers of doublecortin- and Ki67-positive cells, which might aggravate CUMS-induced depressive symptoms. These findings suggest that SELENBP1 might be involved in the regulation of neurogenesis in mice with depression and could be served as a potential target for diagnosing and treating depression.

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Data Availability

Data will be made available from the corresponding author on reasonable request.

Abbreviations

AD:

Alzheimer’s disease

AU:

Arbitrary unit

CAT:

Catalase

CUMS:

Chronic unpredictable mild stress

DCX:

Doublecortin

DG:

Dentate gyrus

GPX:

Glutathione peroxidase

IL-10:

Interleukin 10

IL-1β:

Interleukin 1β

KO:

Knockout

MDA:

Malondialdehyde

ns:

No significance

PD:

Parkinson's disease

ROS:

Reactive oxygen species

SELENBP1:

Selenium binding protein 1

SELENOK:

Selenoprotein K

SELENOP:

Selenoprotein P

SELENOT:

Selenoprotein T

SELENOW:

Selenoprotein W

TGF-β:

Transforming growth factor β

TNF-α:

Tumor necrosis factor-α

WT:

Wild type

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Acknowledgements

The authors would like to thank the Research Center for Basic Sciences of Medicine of Guizhou Medical University for providing large-scale instrument and equipment.

Funding

This work was supported by the National Natural Science Foundation of China [22167008, 21867007, 21561006 and 12132006]; Key Laboratory of Infectious Immune and Antibody Engineering of Guizhou Province [KY [2020]012]; Guizhou Provincial Natural Science Foundation [[2019]1258 and ZK[2023]295]; Opening fund of Hubei Key Laboratory of Bioinorganic Chemistry & Materia Medica [BCMM202002]; Science and Technology Fund of Guizhou Provincial Health Commission [gzwkj2022-514]; Innovation and Entrepreneurship Training program for College students [202110660023]; and the Guizhou Provincial Natural Science Foundation for High-Level Innovative Talents and Teams [2016–5676, 2015–4021].

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Author notes

  1. Yi Jia, Xin Zhang these authors are equally to this paper.

Authors and Affiliations

  1. Key Laboratory of Infectious Immune and Antibody Engineering of Guizhou Province, Cellular Immunotherapy Engineering Research Center of Guizhou Province, School of Biology and Engineering/School of Basic Medical Sciences, Guizhou Medical University, Guiyang, 550025, China

    Yi Jia, Xin Zhang, Yongmei Wang, Yang Liu, Jie Dai, Hongxi Xiang & Zhu Zeng

  2. Immune Cells and Antibody Engineering Research Center of Guizhou Province, Key Laboratory of Biology and Medical Engineering, Guizhou Medical University, Guiyang, 550025, China

    Yi Jia, Xin Zhang, Yongmei Wang, Yang Liu, Jie Dai, Hongxi Xiang & Zhu Zeng

  3. Prenatal Diagnosis Center, Guizhou Provincial People’s Hospital, Guiyang, 550002, Guizhou, China

    Liangliang Zhang & Xian Wu

  4. Department of Laboratory, the Second People’s Hospital of Guizhou Province, Guiyang, 550004, Guizhou, China

    Jie Zhang

  5. Department of Histology and Embryology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, 550025, China

    Yanping Yang

  6. Mental Health Education and Counseling Center for College Students, Guizhou Medical University, Guiyang, 550025, China

    Yulian Chen

  7. Faculty of Psychology, Beijing Normal University, Beijing, 100875, China

    Yulian Chen

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  1. Yi Jia
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Contributions

Yi Jia, Xin Zhang and Yulian Chen: Conceptualization; Yi Jia, Xin Zhang, Yongmei Wang, Yang Liu, Jie Dai, Liangliang Zhang, Xian Wu, Jie Zhang, Hongxi Xiang and Yanping Yang: Methodology; Yi Jia, Jie Dai and Yulian Chen: Validation; Yi Jia, Xin Zhang, Yongmei Wang, Yang Liu Jie Dai, Liangliang Zhang, Xian Wu, Jie Zhang, Hongxi Xiang and Yanping Yang: Data curation; Yi Jia and Xin Zhang: Writing—original draft preparation; Yi Jia, Zhu Zeng and Yulian Chen: Writing—review and editing; Yi Jia, Xin Zhang, Yongmei Wang, Yang Liu and Jie Dai: Visualization; Yi Jia, Jie Dai and Yulian Chen: Supervision; Yi Jia, Jie Dai and Zhu Zeng: Funding acquisition. All authors reviewed the manuscript.

Corresponding author

Correspondence to Yi Jia.

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Competing interests

The authors declare no competing interests.

Ethics Approval

The study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committee of Guizhou Medical University (protocol code: 2021(300), date of approval: 25 March 2021). And the animal study protocol was approved by the Institutional Animal Care and Use Committee at Guizhou Medical University (protocol code 2,100,357, date of approval: 2 March 2021).

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Jia, Y., Zhang, X., Wang, Y. et al. Knocking out Selenium Binding Protein 1 Induces Depressive-Like Behavior in Mice. Biol Trace Elem Res 202, 3149–3162 (2024). https://doi.org/10.1007/s12011-023-03894-8

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