The Alpha 7 Nicotinic Acetylcholine Receptor of Deciduous Dental Pulp Stem Cells Regulates Osteoclastogenesis During Physiological Root Resorption.
The Alpha 7 Nicotinic Acetylcholine Receptor of Deciduous Dental Pulp Stem Cells Regulates Osteoclastogenesis During Physiological Root Resorption.
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DOI：
10.1089/scd.2017.0033
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发表时间：
2017-08
影响因子：
4
通讯作者：
Lulu Wang;Zhifei Zhou;Yujiang Chen;Shuai Yuan;Yang Du;Xinke Ju;Lizheng Wu;Xiaojing Wang
中科院分区：
文献类型：
--
作者：
Lulu Wang;Zhifei Zhou;Yujiang Chen;Shuai Yuan;Yang Du;Xinke Ju;Lizheng Wu;Xiaojing Wang
乳牙生理性牙根吸收是一种正常现象，但其发生机制尚不清楚。本研究从不同吸收阶段的乳牙和正常恒牙中分离出乳牙牙髓干细胞（DDPSCs）和恒牙牙髓干细胞（DPSCs）。在牙根吸收中期，DDPSC诱导破骨细胞分化的能力增强。分泌性哺乳动物Ly-6尿激酶型纤溶酶原激活物受体相关蛋白1（SLURP-1）激活α 7烟碱乙酰胆碱受体（α7 nAChR）导致NF-κB、核因子-κ B配体受体激活物（RANKL）表达水平显著升高，RANKL/骨保护素（OPG）比值显著升高。α-银环蛇毒素（α-BTX）可抑制上述作用。抑制NF-κB后，RANKL/OPG的表达水平明显降低。高强度动态正压可增加稳定期DDPSC中SLURP-1和α7 nAChR的表达。这些数据表明，机械应力刺激DDPSC中SLURP-1和α7 nAChR的表达。此外，SLURP-1激活α7 nAChR，从而上调NF-κB的表达并增强其活性，从而调节RANKL/OPG表达并影响DDPSC影响破骨细胞生成的能力，这可能增强牙根吸收并导致乳牙的生理性丢失。
The physiological root resorption of deciduous teeth is a normal phenomenon, but the mechanisms underlying this process are still unclear. In this study, deciduous dental pulp stem cells (DDPSCs) and permanent dental pulp stem cells (DPSCs) were derived from deciduous teeth and normal permanent teeth at different stages of resorption. In the middle stage of root resorption, DDPSCs exhibited an increase in the ability to induce osteoclast differentiation. Activation of the alpha 7 nicotinic acetylcholine receptor (α7 nAChR) by secretory mammalian Ly-6 urokinase-type plasminogen activator receptor-associated protein 1 (SLURP-1) caused a significant increase in the expression levels of NF-κB, receptor activator of nuclear factor-kappa B ligand (RANKL), and the ratio of RANKL/osteoprotegerin (OPG). These effects were inhibited by alpha-bungarotoxin (α-BTX). Furthermore, the expression levels of RANKL/OPG were significantly reduced following inhibition of NF-κB. High-strength, dynamic positive pressure increased the expression of SLURP-1 and α7 nAChR in DDPSCs in the stable stage. These data indicated that mechanical stress stimulated the expression of SLURP-1 and α7 nAChR in DDPSCs. Additionally, SLURP-1 activated α7 nAChR, thereby upregulating the expression of NF-κB and enhancing its activity, thus regulating RANKL/OPG expression and affecting the ability of DDPSCs to influence osteoclastogenesis, which likely enhances root resorption and leads to the physiological loss of deciduous teeth.