The Effects of Osterix on the Proliferation and Odontoblastic Differentiation of Human Dental Papilla Cells
The Effects of Osterix on the Proliferation and Odontoblastic Differentiation of Human Dental Papilla Cells
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osterix 对人牙乳头细胞增殖和成牙本质细胞分化的影响。
DOI：
10.1016/j.joen.2014.04.012
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发表时间：
2014-11-01
影响因子：
4.2
通讯作者：
Fan, Mingwen
中科院分区：
文献类型：
--
作者：
Yang, Guobin;Li, Xiaoyan;Fan, Mingwen
前言：牙乳头细胞是成牙本质细胞的前体细胞，具有向成牙本质细胞分化的潜能。成骨细胞和成牙本质细胞具有许多共同的特征。Osterix（Osx）是成骨细胞分化所必需的。然而，没有信息可用于Osx对牙本质细胞分化的DPC的影响。本研究旨在探讨Osx对牙源性前体细胞增殖及向成牙本质细胞分化的影响。方法：采用永生化人牙乳头细胞系（hDPC）。Osx在慢病毒颗粒感染的hDPC中稳定过表达或敲低，以确定其对hDPC的生物学效应。用5-乙炔基-2 '-脱氧尿苷掺入法和直接细胞计数法测定细胞增殖。实时荧光定量聚合酶链反应检测牙本质涎磷蛋白、巢蛋白、牙本质基质蛋白1和碱性磷酸酶的表达，以确定细胞的成牙本质细胞分化。采用vonKossa染色和碱性磷酸酶活性测定评价细胞的矿化能力。结果：Osx的过表达抑制hDPCS的增殖，而Osx的敲低则促进hDPCS的增殖。Osx的过表达可通过上调成牙本质细胞分化相关基因的表达，促进hDPC向成牙本质细胞分化，提高hDPC的矿化能力。Osx基因的敲除下调了成牙本质细胞分化相关基因的表达，降低了hDPC的矿化能力。结论：Osx可能是hDPC增殖和向成牙本质细胞分化的潜在调控因子。
Introduction: Dental papilla cells (DPCs) are precursors of odontoblasts and have the potential to differentiate into odontoblasts. Osteoblasts and odontoblasts have many common characteristics. Osterix (Osx) is essential for osteoblast differentiation. However, no information is available for the effects of Osx on the odontoblastic differentiation of DPCs. The purpose of this study was to investigate the effects of Osx on the proliferation and odontoblastic differentiation of DPCs. Methods: An immortalized human dental papilla cell (hDPC) line was used. Osx was stably overexpressed or knocked down in hDPCs with infection of lentiviral particles to determine its biological effects on hDPCs. The proliferation of cells was measured by the 5-ethynyl-2'-deoxyuridine incorporation assay and direct cell counting. Expressions of dentin sialophosphoprotein, nestin, dentin matrix protein 1, and alkaline phosphatase were detected by real-time polymerase chain reaction to determine the odontoblastic differentiation of cells. The mineralization ability of cells was evaluated by von Kossa staining and alkaline phosphatase activity assay. Results: Overexpression of Osx retarded the proliferation of hDPCS, whereas knockdown of Osx increased the cell proliferation. Overexpression of Osx promoted the odontoblastic differentiation of hDPCs by up-regulating odontoblastic differentiation genes and increased the mineralization ability of hDPCs. Knockdown of Osx down-regulated odontoblastic differentiation genes and decreased the mineralization ability of hDPCs. Conclusions: Osx might function as a potential regulator for the proliferation and odontoblastic differentiation of hDPCs.