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β-Catenin Deletion in Regional Neural Progenitors Leads to Congenital Hydrocephalus in Mice 被引量:1
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作者 Lin Ma Yanhua Du +7 位作者 Xiangjie Xu hexi feng Yi Hui Nan Li Guanyu Jiang Xiaoqing Zhang Xiaocui Li Ling Liu 《Neuroscience Bulletin》 SCIE CAS CSCD 2022年第1期81-94,共14页
Congenital hydrocephalus is a major neurological disorder with high rates of morbidity and mortality;however,the underlying cellular and molecular mechanisms remain largely unknown.Reproducible animal models mirroring... Congenital hydrocephalus is a major neurological disorder with high rates of morbidity and mortality;however,the underlying cellular and molecular mechanisms remain largely unknown.Reproducible animal models mirroring both embryonic and postnatal hydrocephalus are also limited.Here,we describe a new mouse model of congenital hydrocephalus through knockout ofβ-catenin in Nkx2.1-expressing regional neural progenitors.Progressive ventriculomegaly and an enlarged brain were consistently observed in knockout mice from embryonic day 12.5 through to adulthood.Transcriptome profiling revealed severe dysfunctions in progenitor maintenance in the ventricular zone and therefore in cilium biogenesis afterβ-catenin knockout.Histological analyses also revealed an aberrant neuronal layout in both the ventral and dorsal telencephalon in hydrocephalic mice at both embryonic and postnatal stages.Thus,knockout ofβ-catenin in regional neural progenitors leads to congenital hydrocephalus and provides a reproducible animal model for studying pathological changes and developing therapeutic interventions for this devastating disease. 展开更多
关键词 Congenital hydrocephalus Β-CATENIN Ependymal cells Nkx2.1 Neural development
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