Heng Boon Chin, Gong Ting, Xu Jianguang, Lim Lee Wei, Zhang Chengfei
Discipline of Endodontology, Faculty of Dentistry, The Prince Philip Dental Hospital, The University of Hong Kong, Hong Kong, SAR, P.R. China.
The University of Hong Kong Shenzhen Institute of Research and Innovation, Shenzhen, Guangdong 518057, P.R. China.
Biomed Rep. 2018 Aug;9(2):161-168. doi: 10.3892/br.2018.1108. Epub 2018 Jun 1.
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.
牙髓干细胞(DPSCs)起源于胚胎神经嵴,具有神经发生潜能。本研究调查了正向和反向 EphrinB2 信号通路在 DPSC 神经发生过程中的作用。在神经诱导培养中,用重组 EphrinB2-Fc 蛋白处理 DPSC 7 天,导致以下神经标志物显著下调:βIII-微管蛋白、神经细胞黏附分子(NCAM)、巢蛋白、神经生成素 2(NGN2)、神经丝中多肽和 Musashi1。免疫细胞化学显示,经 EphrinB2-Fc 处理的 DPSC 表现出更圆的形态,神经突生长较少,同时 βIII-微管蛋白和 NGN2 的蛋白表达降低。用 EphB4 受体特异性肽抑制剂处理 DPSC 显著上调了神经标志物微管相关蛋白 2、Musashi1、NGN2 和神经元特异性烯醇化酶的表达,而用 EphB2 受体特异性肽抑制剂处理对神经发生的影响可忽略不计。EphrinB2 在 DPSC 中的转基因表达导致 Musashi1 和 NCAM 基因表达显著上调,而用重组 EphB4-Fc 蛋白处理 DPSC 仅导致 Musashi1 显著上调。因此,可以得出结论,正向 EphrinB2-EphB4 信号的刺激显著抑制了 DPSC 中的神经发生,而用 EphB4 特异性肽抑制剂抑制该正向信号通路则促进了神经发生。同时,反向 EphB4-EphrinB2 信号的刺激仅略微增强了 DPSC 的神经分化。本研究结果表明 EphrinB2 正向信号的肽或小分子抑制剂在 DPSC 神经组织工程中的潜在应用。