Musashi1 RNA‐binding protein regulates oligodendrocyte lineage cell differentiation and survival
Copyright policy )Musashi1 RNA‐binding protein regulates oligodendrocyte lineage cell differentiation and survival
AbstractExpression of Musashi1 (Msi1), an evolutionarily conserved RNA‐binding protein, in neural stem cells of the subventricular zone in the postnatal and adult CNS indicates a potential role in the generation of oligodendrocytes. We now show Msi1 expression in a subset of oligodendrocyte progenitor (OP) cells in white matter areas temporally and spatially associated with oligodendrogenesis in the postnatal CNS. Msi1 function was evaluated by infection of OP cells with retroviral transduction of Msi1 or knockdown of endogenous Msi1. Retroviral expression of Msi1 significantly reduced the proportion of mature oligodendrocytes generated from OP cells in vitro and in vivo during myelination. Msi1 transduction also promoted OP survival, particularly under conditions of challenge from oxidative stress, while Msi1 siRNA knockdown resulted in dramatic OP cell death. Furthermore, in experimental demyelination Msi1 expression was increased among cells associated with lesions, including OP cells, indicating a potential role in the generation of remyelinating oligodendrocytes. © 2007 Wiley‐Liss, Inc.
- Walter Reed Army Medical Center United States
- Uniformed Services University of the Health Sciences United States
Basic Helix-Loop-Helix Proteins, Male, Cell Survival, Brain, RNA-Binding Proteins, Cell Differentiation, Nerve Tissue Proteins, Original Articles, In Vitro Techniques, Oligodendrocyte Transcription Factor 2, Mice, Inbred C57BL, Disease Models, Animal, Mice, Oligodendroglia, Animals, Newborn, Gene Expression Regulation, Mutation, Animals, RNA, Small Interfering, Cells, Cultured, Cell Proliferation
Basic Helix-Loop-Helix Proteins, Male, Cell Survival, Brain, RNA-Binding Proteins, Cell Differentiation, Nerve Tissue Proteins, Original Articles, In Vitro Techniques, Oligodendrocyte Transcription Factor 2, Mice, Inbred C57BL, Disease Models, Animal, Mice, Oligodendroglia, Animals, Newborn, Gene Expression Regulation, Mutation, Animals, RNA, Small Interfering, Cells, Cultured, Cell Proliferation
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