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The Function of Selenium in Central Nervous System: Lessons from MsrB1 Knockout Mouse Models.

Tengrui Shi1,2, Jianxi Song1, Guanying You1

  • 1Shenzhen Key Laboratory of Marine Biotechnology and Ecology, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518055, China.

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Summary

Methionine sulfoxide reductases (Msr) are crucial for reducing oxidized methionine. MsrB1 deficiency impairs synaptic plasticity and causes astrogliosis in mouse brains, highlighting selenium

Keywords:
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Area of Science:

  • Neurobiology
  • Biochemistry
  • Molecular Biology

Background:

  • MsrB1, initially identified as selenoprotein R, is a methionine sulfoxide reductase (Msr) involved in reducing L-methionine sulfoxide (L-Met-O).
  • The mammalian Msr family includes MsrA and MsrBs (MsrB1, MsrB2, MsrB3), with MsrA reducing L-Met-O (S) epimers and MsrBs reducing L-Met-O (R) epimers in proteins.
  • MsrB1 is the sole mammalian Msr containing selenocysteine, and individual Msr deficiencies lead to distinct phenotypes, suggesting functional non-redundancy.

Purpose of the Study:

  • To review the effects of Msr deficiency on biological functions.
  • To explore the bioactivity of selenium in the central nervous system.
  • To elucidate the role of MsrB1 in neurobiology using a knockout mouse model.

Main Methods:

  • Literature review on Msr family functions and selenium's role in the CNS.
  • Analysis of phenotypes in MsrB1 knockout mouse models.
  • Investigation of synaptic plasticity and astrogliosis in MsrB1-deficient mice.

Main Results:

  • MsrB1 deficiency perturbs synaptic plasticity in mice.
  • Loss of MsrB1 leads to astrogliosis in the brain.
  • MsrB1's unique role in reducing L-Met-O (R) is critical and not fully compensated by other Msrs.

Conclusions:

  • MsrB1 plays a significant role in maintaining brain health and function.
  • Selenium's involvement in L-Met-O reduction is crucial for neurobiology.
  • Further understanding of MsrB1 function is essential for neurodegenerative disease research.