Arthur A, Koblar S, Shi S, Gronthos S
Bone and Cancer Laboratories, Mesenchymal Stem Cell Group, Division of Haematology, Institute of Medical and Veterinary Science, Hanson Institute/University of Adelaide, Frome Road, Adelaide 5000, SA, Australia.
J Dent Res. 2009 Sep;88(9):829-34. doi: 10.1177/0022034509342363.
Damage to the dentin matrix investigates the proliferation and mobilization of dental progenitor cells to the injury site, the mechanisms of which are not defined. EphB receptors and ephrin-B ligands expressed within the perivascular niche of dental pulp have been implicated following tooth injury. We propose that elevated levels of ephrin-B1 following injury may prevent the proliferation and migration of dental pulp stem cell (DPSC), while EphB/ephrin-B interaction facilitates odontoblastic differentiation. The migration, proliferation, and differentiation of DPSC in response to Eph/ephrin-B molecules was assessed in an established ex vivo tooth injury model and by in vitro assays for the assessment of colony formation and differentiation. Analysis of our data demonstrated that EphB forward signaling promoted DPSC proliferation, while inhibiting migration. Conversely, reverse signaling enhanced DPSC mineral production. These observations suggest that EphB/ephrin-B molecules are important for perivascular DPSC migration toward the dentin surfaces and differentiation into functional odontoblasts, following damage to the dentin matrix.
牙本质基质损伤会研究牙源性祖细胞向损伤部位的增殖和迁移情况,但其机制尚不明确。牙齿损伤后,牙髓血管周围微环境中表达的EphB受体和ephrin - B配体被认为与之有关。我们提出,损伤后ephrin - B1水平升高可能会阻止牙髓干细胞(DPSC)的增殖和迁移,而EphB/ephrin - B相互作用则促进成牙本质细胞分化。在已建立的离体牙齿损伤模型中,通过体外集落形成和分化评估试验,评估了DPSC对Eph/ephrin - B分子的迁移、增殖和分化情况。对我们数据的分析表明,EphB正向信号促进DPSC增殖,同时抑制迁移。相反,反向信号增强DPSC矿物质生成。这些观察结果表明,EphB/ephrin - B分子对于牙本质基质损伤后血管周围DPSC向牙本质表面迁移并分化为功能性成牙本质细胞至关重要。