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- W2125573110 abstract "In the developing CNS, Notch1 and its ligand, Jagged1, regulate oligodendrocyte differentiation and myelin formation, but their role in repair of demyelinating lesions in diseases such as multiple sclerosis remains unresolved. To address this question, we generated a mouse model in which we targeted Notch1 inactivation to oligodendrocyte progenitor cells (OPCs) using Olig1 Cre and a floxed Notch1 allele, Notch1 12f . During CNS development, OPC differentiation was potentiated in Olig1 Cre:Notch1 12f/12f mice. Importantly, in adults, remyelination of demyelinating lesions was also accelerated, at the expense of proliferation within the progenitor population. Experiments in vitro confirmed that Notch1 signaling was permissive for OPC expansion but inhibited differentiation and myelin formation. These studies also revealed that astrocytes exposed to TGF-β1 restricted OPC maturation via Jagged1-Notch1 signaling. These data suggest that Notch1 signaling is one of the mechanisms regulating OPC differentiation during CNS remyelination. Thus, Notch1 may represent a potential therapeutical avenue for lesion repair in demyelinating disease." @default.
- W2125573110 created "2016-06-24" @default.
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- W2125573110 date "2009-11-10" @default.
- W2125573110 modified "2023-10-16" @default.
- W2125573110 title "Notch1 signaling plays a role in regulating precursor differentiation during CNS remyelination" @default.
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- W2125573110 doi "https://doi.org/10.1073/pnas.0902834106" @default.
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