A Disintegrin and Metalloprotease 10 in neuronal maturation and gliogenesis during cortex development

作     者：Zhixing Ma Qingyu Li Zhengyu Zhang Yufang Zheng 

作者机构：School of Life Sciences Fudan University 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2013年第8卷第1期

页      面：24-30页

核心收录：

学科分类：0710[理学-生物学] 1002[医学-临床医学] 07[理学] 1001[医学-基础医学(可授医学、理学学位)] 071006[理学-神经生物学] 

基　　金：supported by the National Natural Science Foundation of China,No.30800322 Shanghai Pujiang Program,No.08PJ1401300 Shanghai Leading Academic Discipline Project,No.B111 Ministry of Education Research Fund for New Teachers in Doctoral Program of Higher Educational Institutes,No.200802461050 National Basic Research Program of China(973 Program),No.2011CB503703 Ministry of Education Start Fund to Returned Overseas Scholars Zhuo Xue Program of Fudan University 

主　　题：neural regeneration neurogenesis ADAM10 A Disintegrin and Metalloprotease Notch Notchintracellular domain TujlS100 Nestin cerebral cortex development neuronal maturation glialcell grants-supported paper photographs-containing paper neuroregeneration 

摘      要：The multiple-layer structure of the cerebral cortex is important for its functions. Such a structure is generated based on the proliferation and differentiation of neural stem/progenitor cells. Notch functions as a molecular switch for neural stem/progenitor cell fate during cortex development but the mechanism remains unclear. Biochemical and cellular studies showed that Notch receptor activation induces several proteases to release the Notch intracellular domain （NICD）. A Disintegrin and Metalloprotease 10 （ADAM10） might be a physiological rate-limiting $2 enzyme for Notch activation. Nestin-driven conditional ADAM10 knockout in mouse cortex showed that ADAM10 is cdtical for maintenance of the neural stem cell population during early embryonic cortex development. However, the expression pattern and function of ADAM10 during later cerebral cortex development remains poorly understood. We performed in situ hybridization for ADAMIO mRNA and immunofluorescent analysis to determine the expression of ADAM10 and NICD in mouse cortex from embryonic day 9 （E14.5） to postnatal day 1 （P1）. ADAM10 and NICD were highly co-localized in the cortex of E16.5 to P1 mice. Comparisons of expression patterns of ADAM10 with Nestin （neural stem cell marker）, Tujl （mature neuron marker）, and S100β （gila marker） showed that ADAM10 expression highly matched that of S10013 and partially matched that of Tujl at later embryonic to early postnatal cortex developmental stages. Such expression patterns indicated that ADAM10-Notch signaling might have a critical function in neuronal maturation and gliogenesis during cortex development.