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Activation of the Notch Signaling Pathway and Cellular Localization of Notch Signaling Molecules in the Spinal Cord of SOD1-G93A ALS Model Mice.

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机构： [1]Beijing Geriatric Healthcare Center, Xuanwu Hospital, Capital Medical University, No. 45 Changchun Street, Xicheng, Beijing 100053, China. [2]Department of Neurology, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, Hebei 050000, China [3]Laboratory of Immunology for Environment and Health, Shandong Analysis and Test Center, Qilu University of Technology (Shandong Academy of sciences), Jinan 250014, China [4]Department of scientific research, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, Hebei 050000, China [5]Department of Neurology, Children’s hospital of Hebei province, Shijiazhuang, Hebei 050000, China

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关键词： amyotrophic lateral sclerosis glia Hes1 Jagged1 NICD notch signaling pathway

摘要：

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by motor neuron loss and gliosis in the spinal cord, brain stem and cortex. The Notch signaling pathway has been reported to be dysfunctional in neurodegenerative diseases, including ALS. However, the exact mechanism is still unclear. Here, we detected Notch signaling activation in proliferating glial cells, Notch inactivation in motor neurons in the spinal cord of the SOD1-G93A model, and dramatic changes of cellular relocalization of Notch pathway signaling molecules, including activated Notch intracellular domain (NICD), Notch ligands (Jagged1 and DLL4) and the target gene Hes1. We found that Notch activation was universal in proliferating astrocytes and that the Notch ligand Jagged1 was uniquely upregulated in proliferating microglia, while DLL4 expression was increased in both activated astrocytes and degenerating oligodendrocytes. Our results indicate that microglia may play an important role in the intercellular receptor-ligand interaction of the Notch signaling pathway and contribute to the pathogenesis of motor neuron loss in ALS mice. Further experiments are required to clarify the exact mechanism responsible for Notch dysfunction in ALS. Copyright © 2020 IBRO. Published by Elsevier Ltd. All rights reserved.

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出版当年[2019]版：

大类 | 3 区医学

小类 | 3 区神经科学

最新[2023]版：

大类 | 3 区医学

小类 | 4 区神经科学

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出版当年[2018]版：

Q2 NEUROSCIENCES

最新[2023]版：

Q2 NEUROSCIENCES

影响因子： 2.9 最新[2023版] 3 最新五年平均 3.244 出版当年[2018版] 3.504 出版当年五年平均 3.382 出版前一年[2017版] 3.056 出版后一年[2019版]

第一作者：

第一作者机构： [1]Beijing Geriatric Healthcare Center, Xuanwu Hospital, Capital Medical University, No. 45 Changchun Street, Xicheng, Beijing 100053, China. [2]Department of Neurology, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, Hebei 050000, China [5]Department of Neurology, Children’s hospital of Hebei province, Shijiazhuang, Hebei 050000, China

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通讯机构： [*1]Beijing Geriatric Healthcare Center, Xuanwu Hospital, Capital Medical University, No. 45 Changchun Street, Xicheng, Beijing 100053, China

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Activation of the Notch Signaling Pathway and Cellular Localization of Notch Signaling Molecules in the Spinal Cord of SOD1-G93A ALS Model Mice.

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