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Bull."],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The massive loss of oligodendrocytes caused by various pathological factors is a basic feature of many demyelinating diseases of the central nervous system (CNS). Based on a variety of studies, it is now well established that impairment of oligodendrocyte precursor cells (OPCs) to differentiate and remyelinate axons is a vital event in the failed treatment of demyelinating diseases. Recent evidence suggests that<jats:italic>Foxg1<\/jats:italic>is essential for the proliferation of certain precursors and inhibits premature neurogenesis during brain development. To date, very little attention has been paid to the role of<jats:italic>Foxg1<\/jats:italic>in the proliferation and differentiation of OPCs in demyelinating diseases of the CNS. Here, for the first time, we examined the effects of<jats:italic>Foxg1<\/jats:italic>on demyelination and remyelination in the brain using a cuprizone (CPZ)-induced mouse model. In this work, 7-week-old<jats:italic>Foxg1<\/jats:italic>conditional knockout and wild-type (WT) mice were fed a diet containing 0.2% CPZ w\/w for 5\u00a0weeks, after which CPZ was withdrawn to enable remyelination. Our results demonstrated that, compared with WT mice,<jats:italic>Foxg1<\/jats:italic>-knockout mice exhibited not only alleviated demyelination but also accelerated remyelination of the demyelinated corpus callosum. Furthermore, we found that<jats:italic>Foxg1<\/jats:italic>knockout decreased the proliferation of OPCs and accelerated their differentiation into mature oligodendrocytes both<jats:italic>in vivo<\/jats:italic>and<jats:italic>in vitro<\/jats:italic>. Wnt signaling plays a critical role in development and in a variety of diseases. GSK-3\u03b2, a key regulatory kinase in the Wnt pathway, regulates the ability of \u03b2-catenin to enter nuclei, where it activates the expression of Wnt target genes. We then used SB216763, a selective inhibitor of GSK-3\u03b2 activity, to further demonstrate the regulatory mechanism by which<jats:italic>Foxg1<\/jats:italic>affects OPCs<jats:italic>in vitro<\/jats:italic>. The results showed that SB216763 clearly inhibited the expression of GSK-3\u03b2, which abolished the effect of the proliferation and differentiation of OPCs caused by the knockdown of<jats:italic>Foxg1<\/jats:italic>. These results suggest that<jats:italic>Foxg1<\/jats:italic>is involved in the proliferation and differentiation of OPCs through the Wnt signaling pathway. The present experimental results are some of the first to suggest that<jats:italic>Foxg1<\/jats:italic>is a new therapeutic target for the treatment of demyelinating diseases of the CNS.<\/jats:p>","DOI":"10.1007\/s12264-020-00583-7","type":"journal-article","created":{"date-parts":[[2020,10,5]],"date-time":"2020-10-05T00:03:42Z","timestamp":1601856222000},"page":"15-30","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Conditional Deletion of Foxg1 Alleviates Demyelination and Facilitates Remyelination via the Wnt Signaling Pathway in Cuprizone-Induced Demyelinated Mice"],"prefix":"10.1007","volume":"37","author":[{"given":"Fuxing","family":"Dong","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dajin","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Feiyu","family":"Jiang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yaping","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiuxiang","family":"Wu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xuebin","family":"Qu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jing","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yan","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hongbin","family":"Fan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ruiqin","family":"Yao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2020,10,5]]},"reference":[{"key":"583_CR1","doi-asserted-by":"crossref","first-page":"434","DOI":"10.1007\/s12264-018-0322-7","volume":"35","author":"F Lu","year":"2019","unstructured":"Lu F, Yin D, Pu Y, Liu W, Li Z, Shao Q, et al. 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