Prenatal deletion of DNA methyltransferase 1 in neural stem cells impairs neurogenesis and causes anxiety-like behavior in adulthood

Hirofumi Noguchi, Ayaka Kimura, Naoya Murao, M. Namihira, K. Nakashima
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引用次数: 10

Abstract

ABSTRACT Despite recent advances in our understanding of epigenetic regulation of central nervous system development, little is known regarding the effects of epigenetic dysregulation on neurogenesis and brain function in adulthood. In the present study, we show that prenatal deletion of DNA methyltransferase 1 (Dnmt1) in neural stem cells results in impaired neurogenesis as well as increases in inflammatory features (e.g., elevated glial fibrillary acidic protein [GFAP] expression in astrocytes and increased numbers of microglia) in the adult mouse brain. Moreover, these mice exhibited anxiety-like behavior during an open-field test. These findings suggest that Dnmt1 plays a critical role in regulating neurogenesis and behavior in the developing brain and into adulthood.
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神经干细胞中DNA甲基转移酶1的产前缺失会损害神经发生并导致成年期的焦虑样行为
尽管最近我们对中枢神经系统发育的表观遗传调控的理解取得了进展,但对于表观遗传失调对成年期神经发生和脑功能的影响知之甚少。在本研究中,我们发现神经干细胞中DNA甲基转移酶1 (Dnmt1)的产前缺失会导致成年小鼠大脑中神经发生受损以及炎症特征增加(例如,星形胶质细胞中胶质纤维酸性蛋白[GFAP]表达升高和小胶质细胞数量增加)。此外,这些小鼠在野外测试中表现出焦虑样行为。这些发现表明,Dnmt1在调节发育中的大脑和成年期的神经发生和行为方面起着关键作用。
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