USP9X缺失会增加出生后齿状回内少突胶质细胞的密度

Sabrina Oishi, Oressia H. Zalucki, Susitha Premarathne, S. Wood, M. Piper
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引用次数: 6

摘要

成人海马齿状回内的神经干细胞(NSCs)位于亚颗粒区(SGZ)。一个动态的信号机制网络控制着NSC身份维持和随后向齿状颗粒神经元分化之间的平衡。最近,泛素特异性蛋白酶9x -linked (USP9X)被证明对海马形态发生很重要,因为缺乏该基因的小鼠在出生后齿状回中表现出更高比例的增殖性NSCs,但神经元数量减少。在这里,我们揭示了usp9x缺乏导致出生后海马中许多少突胶质细胞和髓磷脂相关基因的上调。此外,细胞计数显示突变体齿状回单位体积的少突胶质细胞前体细胞和成熟少突胶质细胞显著增加。总的来说,这些发现表明USP9X可能调节出生后SGZ内的NSC谱系决定。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
USP9X deletion elevates the density of oligodendrocytes within the postnatal dentate gyrus
ABSTRACT Neural stem cells (NSCs) within the adult hippocampal dentate gyrus reside in the subgranular zone (SGZ). A dynamic network of signaling mechanisms controls the balance between the maintenance of NSC identity, and their subsequent differentiation into dentate granule neurons. Recently, the ubiquitin-specific protease 9 X-linked (USP9X) was shown to be important for hippocampal morphogenesis, as mice lacking this gene exhibited a higher proportion of proliferating NSCs, yet a decrease in neuronal numbers, within the postnatal dentate gyrus. Here we reveal that Usp9x-deficiency results in the upregulation of numerous oligodendrocytic and myelin-associated genes within the postnatal hippocampus. Moreover, cell counts reveal a significant increase in oligodendrocyte precursor cells and mature oligodendrocytes per unit volume of the mutant dentate gyrus. Collectively, these findings indicate that USP9X may regulate NSC lineage determination within the postnatal SGZ.
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