VIP Center, School and Hospital of Stomatology, Shandong University, Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Jinan, China.
VIP Center, School and Hospital of Stomatology, Shandong University, Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Jinan, China; Department of Endodontics, Jinan Stomatological Hospital, Jinan, China.
J Endod. 2019 Feb;45(2):161-167. doi: 10.1016/j.joen.2018.10.009.
Odontogenic differentiation of human stem cells from the apical papilla (SCAPs) is a prerequisite step in the root development of immature permanent teeth. However, little is known about the effects of an inflammatory environment on osteo/odontogenic differentiation of SCAPs. The purpose of this study was to investigate the effects of lipopolysaccharide (LPS) on the proliferation and osteo/odontogenic differentiation of SCAPs and the role of mitogen-activated protein kinase (MAPK) signaling pathways in LPS-mediated osteo/odontogenic differentiation of SCAPs.
SCAPs of human third permanent molars were cultured. Cell viability was analyzed. Alkaline phosphatase activity and mineralization ability were investigated. Gene expression of osteo/odontogenic differentiation and MAPK signaling pathways was evaluated during osteo/odontogenic differentiation of SCAPs.
In the 0.1 μg/mL LPS-treated group, cell proliferation, alkaline phosphatase activity, and mineralization of SCAPs were up-regulated. Real-time quantitative polymerase chain reaction revealed that dentin sialophosphoprotein, runt-related transcription factor 2, and bone sialoprotein were increased. However, we did not detect any change of osteocalcin expression. In addition, the expression of p-ERK and p-p38 in SCAPs was enhanced by LPS treatment, whereas the inhibition of ERK and p38 MAPK pathways markedly suppressed the differentiation of LPS-treated SCAPs.
Our findings showed that LPS at the appropriate concentration promoted the proliferation and osteo/odontogenic differentiation of SCAPs. ERK and p38 MAPK signaling pathways are involved in LPS-mediated osteo/odontogenic differentiation of SCAPs.
人根尖乳头干细胞（SCAPs）的牙源性分化是未成熟恒牙牙根发育的前提步骤。然而，人们对炎性环境对 SCAPs 的成骨/成牙分化的影响知之甚少。本研究旨在探讨脂多糖（LPS）对 SCAPs 增殖和成骨/成牙分化的影响，以及丝裂原活化蛋白激酶（MAPK）信号通路在 LPS 介导的 SCAPs 成骨/成牙分化中的作用。
培养人第三磨牙的 SCAPs。分析细胞活力。研究碱性磷酸酶活性和矿化能力。评估 SCAPs 成骨/成牙分化过程中 MAPK 信号通路和基因表达的变化。
在 0.1μg/mL LPS 处理组中，SCAPs 的细胞增殖、碱性磷酸酶活性和矿化能力上调。实时定量聚合酶链反应显示牙本质涎磷蛋白、 runt 相关转录因子 2 和骨涎蛋白增加。然而，我们没有检测到骨钙素表达的任何变化。此外，LPS 处理增强了 SCAPs 中 p-ERK 和 p-p38 的表达，而 ERK 和 p38 MAPK 通路的抑制显著抑制了 LPS 处理的 SCAPs 的分化。
我们的研究结果表明，适当浓度的 LPS 促进了 SCAPs 的增殖和成骨/成牙分化。ERK 和 p38 MAPK 信号通路参与 LPS 介导的 SCAPs 成骨/成牙分化。
