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Possible role of EphA4 and VEGFR2 interactions in neural stem and progenitor cell differentiation

  • Authors:
    • Qingfa Chen
    • Jia Liu
    • Takahiro Sawada
    • Chuanfei Wei
    • Shichao Wu
    • Fabin Han
  • View Affiliations / Copyright

    Affiliations: Centre for Tissue Engineering and Regenerative Medicine, Liaocheng People's Hospital, Liaocheng University, Liaocheng, Shandong 252000, P.R. China, Department of Neurology, Liaocheng People's Hospital, Liaocheng University, Liaocheng, Shandong 252000, P.R. China, Department of Molecular Cell Biology and Molecular Medicine, Institute of Advanced Medicine, Wakayama Medical University, Kimiidera, Wakayama 641‑8509, Japan
    Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1789-1796
    |
    Published online on: January 3, 2020
       https://doi.org/10.3892/etm.2020.8419
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Abstract

Neural stem and progenitor cells (NSPCs) are important pluripotent stem cells, which have potential applications for cell replacement therapy. Ephrin receptors (Ephs) and angiogenic growth factor receptors have a major impact on the proliferation and differentiation of NSPCs. Potential interactions between EphA4 and vascular endothelial growth factor (VEGF) receptor (VEGFR) 2, and their roles in NSPC differentiation in vitro remain unknown. In the present study, mouse embryonic NSPCs were treated with ephrin‑A1 or VEGF165 alone as well as with combination treatment (ephrin‑A1 + VEGF165). Immunoprecipitation and immunoblot assays demonstrated that wild‑type EphA4, but not the EphA4 kinase‑dead mutant, interacted with VEGFR2 when overexpressed in 293T cells. This interaction was inhibited by dominant‑negative EphA4. The percentage of β‑tubulin III (Tuj1)+, but not glial fibrillary acid protein (GFAP)+ cells, was increased in the ephrin‑A1 + VEGF165 combination group as compared to the VEGF165 alone group in mouse embryonic NSPCs. VEGF165‑induced neuronal differentiation was potentiated by ephrin‑A1 in NSPCs in vitro and ephrin‑A1‑ or VEGF165‑stimulated EphA4 and VEGFR2 interactions may mediate the signaling pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Chen Q, Liu J, Sawada T, Wei C, Wu S and Han F: Possible role of EphA4 and VEGFR2 interactions in neural stem and progenitor cell differentiation. Exp Ther Med 19: 1789-1796, 2020.
APA
Chen, Q., Liu, J., Sawada, T., Wei, C., Wu, S., & Han, F. (2020). Possible role of EphA4 and VEGFR2 interactions in neural stem and progenitor cell differentiation. Experimental and Therapeutic Medicine, 19, 1789-1796. https://doi.org/10.3892/etm.2020.8419
MLA
Chen, Q., Liu, J., Sawada, T., Wei, C., Wu, S., Han, F."Possible role of EphA4 and VEGFR2 interactions in neural stem and progenitor cell differentiation". Experimental and Therapeutic Medicine 19.3 (2020): 1789-1796.
Chicago
Chen, Q., Liu, J., Sawada, T., Wei, C., Wu, S., Han, F."Possible role of EphA4 and VEGFR2 interactions in neural stem and progenitor cell differentiation". Experimental and Therapeutic Medicine 19, no. 3 (2020): 1789-1796. https://doi.org/10.3892/etm.2020.8419
Copy and paste a formatted citation
x
Spandidos Publications style
Chen Q, Liu J, Sawada T, Wei C, Wu S and Han F: Possible role of EphA4 and VEGFR2 interactions in neural stem and progenitor cell differentiation. Exp Ther Med 19: 1789-1796, 2020.
APA
Chen, Q., Liu, J., Sawada, T., Wei, C., Wu, S., & Han, F. (2020). Possible role of EphA4 and VEGFR2 interactions in neural stem and progenitor cell differentiation. Experimental and Therapeutic Medicine, 19, 1789-1796. https://doi.org/10.3892/etm.2020.8419
MLA
Chen, Q., Liu, J., Sawada, T., Wei, C., Wu, S., Han, F."Possible role of EphA4 and VEGFR2 interactions in neural stem and progenitor cell differentiation". Experimental and Therapeutic Medicine 19.3 (2020): 1789-1796.
Chicago
Chen, Q., Liu, J., Sawada, T., Wei, C., Wu, S., Han, F."Possible role of EphA4 and VEGFR2 interactions in neural stem and progenitor cell differentiation". Experimental and Therapeutic Medicine 19, no. 3 (2020): 1789-1796. https://doi.org/10.3892/etm.2020.8419
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