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

Yi Jia1,2, Xin Zhang3,4, Yongmei Wang3,4

  • 1Key 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. jiayiyouxiang@163.com.

Biological Trace Element Research
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PubMed
Summary
This summary is machine-generated.

Selenium binding protein 1 (SELENBP1) levels decrease in depression, impacting neurogenesis. SELENBP1 deficiency worsens depressive behavior and neuroinflammation, suggesting SELENBP1 as a potential diagnostic and therapeutic target for depression.

Keywords:
Depressive-like behaviorInflammatory cytokinesNeurogenesisOxidative stressSelenium binding protein 1

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Selenium binding protein 1 (SELENBP1) is implicated in various neurological disorders.
  • The specific role of SELENBP1 in depression and its associated mechanisms of oxidative stress and inflammation are not well understood.

Purpose of the Study:

  • To investigate the expression levels of SELENBP1 in a mouse model of depression and in human patients with depression.
  • To explore the impact of SELENBP1 knockout on inflammation, oxidative stress, and hippocampal neurogenesis in a depression model.

Main Methods:

  • Analysis of SELENBP1 expression in the hippocampus of a mouse depression model and serum of human patients using the Gene Expression Omnibus database.
  • Validation using blood samples from human patients and chronic unpredictable mild stress (CUMS)-induced mouse models.
  • Assessment of SELENBP1 knockout effects on depressive behavior, inflammatory cytokines, oxidative stress markers, and neurogenesis (doublecortin and Ki67 staining).

Main Results:

  • SELENBP1 expression was found to be decreased in the blood of human patients and the hippocampus of mice with depression.
  • SELENBP1 knockout exacerbated CUMS-induced depressive behavior in mice.
  • SELENBP1 deficiency led to dysregulation of inflammatory cytokines and oxidative stress, and reduced hippocampal neurogenesis.

Conclusions:

  • SELENBP1 plays a role in regulating neurogenesis in depression.
  • Decreased SELENBP1 levels may contribute to the pathophysiology of depression.
  • SELENBP1 represents a potential biomarker for depression diagnosis and a therapeutic target for treatment.