Accumulated quiescent neural stem cells in adult hippocampus of the mouse model for the MECP2 duplication syndrome

被引:17
作者
Chen, Zhifang [1 ]
Li, Xiao [1 ]
Zhou, Jingjing [2 ]
Yuan, Bo [1 ]
Yu, Bin [1 ]
Tong, Dali [1 ]
Cheng, Cheng [1 ]
Shao, Yinqi [1 ]
Xia, Shengnan [1 ]
Zhang, Ran [1 ]
Lyu, Jingwen [2 ]
Yu, Xiuya [2 ]
Dong, Chen [2 ]
Zhou, Wen-Hao [2 ]
Qiu, Zilong [1 ]
机构
[1] Chinese Acad Sci, CAS Ctr Excellence Brain Sci & Intelligence Tech, Shanghai Inst Biol Sci, Inst Neurosci,CAS Key Lab Primate Neurobiol,State, 320 Yue Yang Rd, Shanghai 200031, Peoples R China
[2] Fudan Univ, Dept Neonatol, Childrens Hosp, Shanghai 201102, Peoples R China
来源
SCIENTIFIC REPORTS | 2017年 / 7卷
关键词
RETT-SYNDROME; NEUROGENESIS; DISORDER; ABSENCE;
D O I
10.1038/srep41701
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Duplications of Methyl CpG binding protein 2 (MECP2) -containing segments lead to the MECP2 duplication syndrome, in which severe autistic symptoms were identified. Whether adult neurogenesis may play a role in pathogenesis of autism and the role of MECP2 on state determination of adult neural stem cells (NSCs) remain largely unclear. Using a MECP2 transgenic (TG) mouse model for the MECP2 duplication syndrome, we found that adult hippocampal quiescent NSCs were significantly accumulated in TG mice comparing to wild type (WT) mice, the neural progenitor cells (NPCs) were reduced and the neuroblasts were increased in adult hippocampi of MECP2 TG mice. Interestingly, we found that parvalbumin (PV) positive interneurons were significantly decreased in MECP2 TG mice, which were critical for determining fates of adult hippocampal NSCs between the quiescence and activation. In summary, we found that MeCP2 plays a critical role in regulating fate determination of adult NSCs. These evidences further suggest that abnormal development of NSCs may play a role in the pathogenesis of the MECP2 duplication syndrome.
引用
收藏
页数:9
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