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

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 t...

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Autores principales: Ma, Zhixing, Li, Qingyu, Zhang, Zhengyu, Zheng, Yufang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4107504/
https://www.ncbi.nlm.nih.gov/pubmed/25206368
http://dx.doi.org/10.3969/j.issn.1673-5374.2013.01.003
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author Ma, Zhixing
Li, Qingyu
Zhang, Zhengyu
Zheng, Yufang
author_facet Ma, Zhixing
Li, Qingyu
Zhang, Zhengyu
Zheng, Yufang
author_sort Ma, Zhixing
collection PubMed
description 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 S2 enzyme for Notch activation. Nestin-driven conditional ADAM10 knockout in mouse cortex showed that ADAM10 is critical 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 ADAM10 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), Tuj1 (mature neuron marker), and S100β (glia marker) showed that ADAM10 expression highly matched that of S100β and partially matched that of Tuj1 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.
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spelling pubmed-41075042014-09-09 A Disintegrin and Metalloprotease 10 in neuronal maturation and gliogenesis during cortex development Ma, Zhixing Li, Qingyu Zhang, Zhengyu Zheng, Yufang Neural Regen Res Research and Report Article: Neurogenesis and Neural Plasticity and Neural Regeneration 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 S2 enzyme for Notch activation. Nestin-driven conditional ADAM10 knockout in mouse cortex showed that ADAM10 is critical 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 ADAM10 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), Tuj1 (mature neuron marker), and S100β (glia marker) showed that ADAM10 expression highly matched that of S100β and partially matched that of Tuj1 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. Medknow Publications & Media Pvt Ltd 2013-01-05 /pmc/articles/PMC4107504/ /pubmed/25206368 http://dx.doi.org/10.3969/j.issn.1673-5374.2013.01.003 Text en Copyright: © Neural Regeneration Research http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research and Report Article: Neurogenesis and Neural Plasticity and Neural Regeneration
Ma, Zhixing
Li, Qingyu
Zhang, Zhengyu
Zheng, Yufang
A Disintegrin and Metalloprotease 10 in neuronal maturation and gliogenesis during cortex development
title A Disintegrin and Metalloprotease 10 in neuronal maturation and gliogenesis during cortex development
title_full A Disintegrin and Metalloprotease 10 in neuronal maturation and gliogenesis during cortex development
title_fullStr A Disintegrin and Metalloprotease 10 in neuronal maturation and gliogenesis during cortex development
title_full_unstemmed A Disintegrin and Metalloprotease 10 in neuronal maturation and gliogenesis during cortex development
title_short A Disintegrin and Metalloprotease 10 in neuronal maturation and gliogenesis during cortex development
title_sort disintegrin and metalloprotease 10 in neuronal maturation and gliogenesis during cortex development
topic Research and Report Article: Neurogenesis and Neural Plasticity and Neural Regeneration
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4107504/
https://www.ncbi.nlm.nih.gov/pubmed/25206368
http://dx.doi.org/10.3969/j.issn.1673-5374.2013.01.003
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