Mice lacking BCAS1, a novel myelin-associated protein, display hypomyelination, schizophrenia-like abnormal behaviors, and upregulation of inflammatory genes in the brain

Tetsuya Ishimoto, Kensuke Ninomiya, Ran Inoue, Masato Koike, Yasuo Uchiyama, Hisashi Mori*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

44 Scopus citations

Abstract

The abnormal expression and function of myelin-related proteins contribute to nervous system dysfunction associated with neuropsychiatric disorders; however, the underlying mechanism of this remains unclear. We found here that breast carcinoma amplified sequence 1 (BCAS1), a basic protein abundant in the brain, was expressed specifically in oligodendrocytes and Schwann cells, and that its expression level was decreased by demyelination. This suggests that BCAS1 is a novel myelin-associated protein. BCAS1 knockout mice displayed schizophrenia-like behavioral abnormalities and a tendency toward reduced anxiety-like behaviors. Moreover, we found that the loss of BCAS1 specifically induced hypomyelination and the expression of inflammation-related genes in the brain. These observations provide a novel insight into the functional link between oligodendrocytes and inflammation and/or abnormal behaviors.

Original languageEnglish
Pages (from-to)727-739
Number of pages13
JournalGLIA
Volume65
Issue number5
DOIs
StatePublished - 2017/05/01

Keywords

  • Schwann cells
  • hypomyelination
  • knockout mouse
  • oligodendrocyte
  • schizophrenia

ASJC Scopus subject areas

  • Neurology
  • Cellular and Molecular Neuroscience

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