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• W3037647673 abstract "Slit1 is a secreted axon guidance molecule, also involved in adult neurogenesis. In physiological conditions, Slit1 loss promotes ectopic dispersal of SVZ-derived neural precursors (SVZ-NPCs) into periventricular structures such as the corpus callosum. Demyelination of the corpus callosum triggers SVZ-NPC migration to ectopic locations and their recruitment by the lesion, suggesting a possible role for Slit1 in SVZ-NPCs ectopic dispersal regulation in pathological conditions. Here, we have investigated the function of Slit1 protein in the recruitment of SVZ-NPCs after CNS demyelination. We find that the dynamics of oligodendrogenesis and temporal profile of developmental myelination in Slit1-/- mice are similar to Slit1+/- controls. SVZ micro-dissection and RT-PCR from wild-type mice, show that Slits and Robos are physiologically regulated at the transcriptional level in response to corpus callosum demyelination suggesting their role in the process of SVZ-NPC ectopic migration in demyelinating conditions. Moreover, we find that the number of SVZ-NPCs recruited by the lesion increases in Sli1-/- mice compared to Slit1+/- mice, leading to higher numbers of Olig2+ cells within the lesion. Time-lapse video-microscopy of immuno-purified NPCs shows that Slit1-deficient cells migrate faster and make more frequent directional changes than control NPCs, supporting a cell-autonomous mechanism of action of Slit1 in NPC migration. In conclusion, while Slit1 does not affect the normal developmental process of oligodendrogenesis and myelination, it regulates adult SVZ-NPC ectopic migration in response to demyelination, and consequently oligodendrocyte renewal within the lesion." @default.
• W3037647673 created "2020-07-02" @default.
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• W3037647673 date "2020-06-26" @default.
• W3037647673 modified "2023-10-18" @default.
• W3037647673 title "Slit1 Protein Regulates SVZ-Derived Precursor Mobilization in the Adult Demyelinated CNS" @default.
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• W3037647673 doi "https://doi.org/10.3389/fncel.2020.00168" @default.
• W3037647673 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7332780" @default.
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• W3037647673 hasPublicationYear "2020" @default.
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