Recruitment of mesenchymal stem cells by stromal cell-derived factor 1α in pulp cells from deciduous teeth
Recruitment of mesenchymal stem cells by stromal cell-derived factor 1α in pulp cells from deciduous teeth
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DOI：
10.3892/ijmm.2015.2247
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发表时间：
2015-08-01
影响因子：
5.4
通讯作者：
Iwamoto, Tsutomu
中科院分区：
文献类型：
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作者：
Akazawa, Yuki;Hasegawa, Tomokazu;Iwamoto, Tsutomu
牙髓细胞（DPC），包括牙髓（DP）干细胞，在某些条件下由龋齿，牙齿骨折和损伤相关的细菌感染引起的牙本质修复中发挥作用。间充质干细胞（MSC）也被证明参与了这一修复过程。然而，MSC被募集到DP的机制尚未阐明。因此，本体外研究的目的是研究基质细胞衍生因子1 α（SDF 1）-C-X-C趋化因子受体4型（CXCR 4）信号传导是否参与乳牙DP的组织修复。将来自DPC（SDP 11）和UE 7 T-13细胞的单细胞克隆分别用作牙髓细胞和MSC。以MG-63和HuO 9两种骨肉瘤细胞系作为阳性对照细胞。逆转录聚合酶链反应（RT-PCR）显示所有细胞系（SDP 11、UE 7 T-13、MG-63和HuO 9）均表达SDF 1和CXCR 4 mRNA。免疫细胞化学分析表明，SDF 1和CXCR 4蛋白在SDP 11和UE 7 T-13细胞中均有表达。在从SDP 11和UE 7 T-13细胞收集的细胞裂解物（CL）和条件培养基（CM）中也检测到SDF 1，CXCR 4的特异性拮抗剂AMD 3100抑制UE 7 T-13细胞的迁移;该迁移由从SDP 11细胞收集的CM处理诱导。此外，实时PCR显示，用20 ng/ml成纤维细胞生长因子（FGF）-2处理可抑制SDP 11细胞中SDF 1的表达，而暴露于FGF受体抑制剂AZD 4547可阻断这种抑制作用。总的来说，这些数据表明，DP产生的SDF 1通过招募MSC在体内平衡、修复和再生中发挥着重要作用。
Dental pulp cells (DPCs), including dental pulp (DP) stem cells, play a role in dentine repair under certain conditions caused by bacterial infections associated with caries, tooth fracture and injury. Mesenchymal stem cells (MSCs) have also been shown to be involved in this process of repair. However, the mechanisms through which MSCs are recruited to the DP have not yet been elucidated. Therefore, the aim of the present in vitro study was to investigate whether stromal cell-derived factor 1 alpha (SDF1)-C-X-C chemokine receptor type 4 (CXCR4) signaling is involved in tissue repair in the DP of deciduous teeth. A single-cell clone from DPCs (SDP11) and UE7T-13 cells were used as pulp cells and MSCs, respectively. The MG-63 and HuO9 cells, two osteosarcoma cell lines, were used as positive control cells. Reverse transcription polymerase chain reaction (RT-PCR) revealed that all cell lines (SDP11, UE7T-13 MG-63 and HuO9) were positive for both SDF1 and CXCR4 mRNA expression. Moreover, immunocytochemical analysis indicated that SDF1 and CXCR4 proteins were expressed in the SDP11 and UE7T-13 cells. SDF1 was also detected in the cell lysates (CLs) and conditioned medium (CM) collected from the SDP11 and UE7T-13 cells, and AMD3100, a specific antagonist of CXCR4, inhibited the migration of the UE7T-13 cells; this migration was induced by treatment with CM, which was collected from the SDP11 cells. In addition, real-time PCR showed that the expression of SDF1 in the SDP11 cells was inhibited by treatment with 20 ng/ml fibroblast growth factor (FGF)-2, and exposure to AZD4547, an inhibitor of the FGF receptor, blocked this inhibition. Collectively, these data suggest that SDF1 produced by DP plays an important role in homeostasis, repair and regeneration via the recruitment of MSCs.