SDF-1/CXCR4 Signaling Maintains Stemness Signature in Mouse Neural Stem/Progenitor Cells

SDF-1 and its primary receptor, CXCR4, are highly expressed in the embryonic central nervous system (CNS) and play a crucial role in brain architecture. Loss of SDF-1/CXCR4 signaling causes abnormal development of neural stem/progenitor cells (NSCs/NPCs) in the cerebellum, hippocampus, and cortex. H...

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Bibliographic Details
Published in:Stem Cells International 2017-01, Vol.2017 (2017), p.1-14-045
Main Authors: Liou, Horng-Huei, Lai, Dar-Ming, Lee, Sue-Wei, Chen, I-Chun, Liu, Fei-Chih, Liou, Jeffrey Tsai-Jui, Lin, Hsing-Yu, Ling, Thai-Yen, Ho, Shih-Yin, Hsu, Yu
Format: Article
Language:English
Subjects:
Analysis
Brain
Cell cycle
Cell differentiation
Cellular signal transduction
Chemokine receptors
Chemokines
Epidermal growth factor
Gene expression
Genes
Genetic engineering
Hospitals
Immunoglobulins
Kinases
Medical research
Medicine
Neurogenesis
Physiology
Stem cells
Studies
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Summary:SDF-1 and its primary receptor, CXCR4, are highly expressed in the embryonic central nervous system (CNS) and play a crucial role in brain architecture. Loss of SDF-1/CXCR4 signaling causes abnormal development of neural stem/progenitor cells (NSCs/NPCs) in the cerebellum, hippocampus, and cortex. However, the mechanism of SDF-1/CXCR4 axis in NSCs/NPCs regulation remains unknown. In this study, we found that elimination of SDF-1/CXCR4 transduction caused NSCs/NPCs to lose their stemness characteristics and to encounter neurogenic differentiation. Moreover, Notch and RE1 silencing transcription factor (REST) both play an essential role in NSCs/NPCs maintenance and neuronal differentiation and were dramatically downregulated following SDF-1/CXCR4 cascade inhibition. Finally, we demonstrated that the expression of achaete-scute homolog 1 (Ascl1), a proneural gene, and p27, an antiproliferative gene, were significantly increased after genetic elimination of SDF-1 alleles. Our results support that the loss of functional SDF-1/CXCR4 signaling pathway in NSCs/NPCs induces exit of cell cycle and promotes premature neural differentiation.
ISSN:1687-966X
1687-9678
1687-9678
DOI:10.1155/2017/2493752