Wnt5a Promotes Cortical Neuron Survival by Inhibiting Cell-Cycle Activation

β-Amyloid protein (Aβ) is thought to cause neuronal loss in Alzheimer's disease (AD). Aβ treatment promotes the re-activation of a mitotic cycle and induces rapid apoptotic death of neurons. However, the signaling pathways mediating cell-cycle activation during neuron apoptosis have not been de...

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Bibliographic Details
Published in:Frontiers in cellular neuroscience 2017-09, Vol.11, p.281-281
Main Authors: Zhou, Li, Chen, Di, Huang, Xu-Ming, Long, Fei, Cai, Hua, Yao, Wen-Xia, Chen, Zhong-Cheng, Liao, Zhi-Jian, Deng, Zhe-Zhi, Tan, Sha, Shan, Yi-Long, Cai, Wei, Wang, Yu-Ge, Yang, Ri-Hong, Jiang, Nan, Peng, Tao, Hong, Ming-Fan, Lu, Zheng-Qi
Format: Article
Language:English
Subjects:
Alzheimer's disease
Apoptosis
Binding sites
Calcium
Cell activation
Cell cycle
Cell survival
cell-cycle activation
Clinical medicine
cortical neuron
Cyclin D1
Cyclin-dependent kinases
Gene expression
Hospitals
Immunology
Kinases
Laboratories
Mutation
Neurodegeneration
Neurons
Neuroscience
Pathology
Penicillin
Peptides
Signal transduction
Wnt protein
Wnt5a
β-Amyloid
β-Amyloid protein
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Summary:β-Amyloid protein (Aβ) is thought to cause neuronal loss in Alzheimer's disease (AD). Aβ treatment promotes the re-activation of a mitotic cycle and induces rapid apoptotic death of neurons. However, the signaling pathways mediating cell-cycle activation during neuron apoptosis have not been determined. We find that Wnt5a acts as a mediator of cortical neuron survival, and Aβ promotes cortical neuron apoptosis by downregulating the expression of Wnt5a. Cell-cycle activation is mediated by the reduced inhibitory effect of Wnt5a in Aβ treated cortical neurons. Furthermore, Wnt5a signals through the non-canonical Wnt/Ca pathway to suppress cyclin D1 expression and negatively regulate neuronal cell-cycle activation in a cell-autonomous manner. Together, aberrant downregulation of Wnt5a signaling is a crucial step during Aβ induced cortical neuron apoptosis and might contribute to AD-related neurodegeneration.
ISSN:1662-5102
1662-5102
DOI:10.3389/fncel.2017.00281