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Article

EphrinB2 signalling modulates the neural differentiation of human dental pulp stem cells

  • Authors:
    • Boon Chin Heng
    • Ting Gong
    • Jianguang Xu
    • Lee Wei Lim
    • Chengfei Zhang
  • View Affiliations / Copyright

    Affiliations: Discipline of Endodontology, Faculty of Dentistry, The Prince Philip Dental Hospital, The University of Hong Kong, Hong Kong, SAR, P.R. China, Faculty of Science and Technology, Sunway University, Selangor Darul Ehsan 47500, Malaysia
  • Pages: 161-168
    |
    Published online on: June 1, 2018
       https://doi.org/10.3892/br.2018.1108
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Abstract

Dental pulp stem cells (DPSCs) originate from the embryonic neural crest and have neurogenic potential. The present study investigated the roles of the forward and reverse EphrinB2 signalling pathways during DPSC neurogenesis. Treatment of DPSCs with recombinant EphrinB2‑Fc protein over 7 days in a neural induction culture resulted in significant downregulation of the following neural markers: βIII‑Tubulin, neural cell adhesion molecule (NCAM), nestin, neurogenin 2 (NGN2), neurofilament medium polypeptide and Musashi1. Immunocytochemistry revealed that EphrinB2‑Fc‑treated DPSCs exhibited more rounded morphologies with fewer neurite outgrowths as well as reduced protein expression of βIII‑tubulin and NGN2. Treatment of DPSCs with a peptide inhibitor specific to the EphB4 receptor significantly upregulated expression of the neural markers microtubule‑associated protein 2, Musashi1, NGN2 and neuron‑specific enolase, whereas treatment with a peptide inhibitor specific to the EphB2 receptor exerted negligible effects on neurogenesis. Transgenic expression of EphrinB2 in DPSCs resulted in significant upregulation of Musashi1 and NCAM gene expression, while treatment of DPSCs with recombinant EphB4‑Fc protein led to significant upregulation of only Musashi1. Thus, it may be concluded that stimulation of forward EphrinB2‑EphB4 signalling markedly inhibited neurogenesis in DPSCs, whereas suppression of this forward signalling pathway with peptide inhibitor specific to EphB4 promoted neurogenesis. Meanwhile, stimulation of reverse EphB4‑EphrinB2 signalling only marginally enhanced the neural differentiation of DPSCs. The present findings indicate the potential application of peptide or small molecule inhibitors of EphrinB2 forward signalling in neural tissue engineering with DPSCs.
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Copy and paste a formatted citation
Spandidos Publications style
Heng BC, Gong T, Xu J, Lim L and Zhang C: EphrinB2 signalling modulates the neural differentiation of human dental pulp stem cells. Biomed Rep 9: 161-168, 2018.
APA
Heng, B.C., Gong, T., Xu, J., Lim, L., & Zhang, C. (2018). EphrinB2 signalling modulates the neural differentiation of human dental pulp stem cells. Biomedical Reports, 9, 161-168. https://doi.org/10.3892/br.2018.1108
MLA
Heng, B. C., Gong, T., Xu, J., Lim, L., Zhang, C."EphrinB2 signalling modulates the neural differentiation of human dental pulp stem cells". Biomedical Reports 9.2 (2018): 161-168.
Chicago
Heng, B. C., Gong, T., Xu, J., Lim, L., Zhang, C."EphrinB2 signalling modulates the neural differentiation of human dental pulp stem cells". Biomedical Reports 9, no. 2 (2018): 161-168. https://doi.org/10.3892/br.2018.1108
Copy and paste a formatted citation
x
Spandidos Publications style
Heng BC, Gong T, Xu J, Lim L and Zhang C: EphrinB2 signalling modulates the neural differentiation of human dental pulp stem cells. Biomed Rep 9: 161-168, 2018.
APA
Heng, B.C., Gong, T., Xu, J., Lim, L., & Zhang, C. (2018). EphrinB2 signalling modulates the neural differentiation of human dental pulp stem cells. Biomedical Reports, 9, 161-168. https://doi.org/10.3892/br.2018.1108
MLA
Heng, B. C., Gong, T., Xu, J., Lim, L., Zhang, C."EphrinB2 signalling modulates the neural differentiation of human dental pulp stem cells". Biomedical Reports 9.2 (2018): 161-168.
Chicago
Heng, B. C., Gong, T., Xu, J., Lim, L., Zhang, C."EphrinB2 signalling modulates the neural differentiation of human dental pulp stem cells". Biomedical Reports 9, no. 2 (2018): 161-168. https://doi.org/10.3892/br.2018.1108
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