Intermittent Administration of Parathyroid Hormone Enhances Odonto/Osteogenic Differentiation of Stem Cells from the Apical Papilla via JNK and P38 MAPK Pathways.
Intermittent Administration of Parathyroid Hormone Enhances Odonto/Osteogenic Differentiation of Stem Cells from the Apical Papilla via JNK and P38 MAPK Pathways.
复制标题
间歇性施用甲状旁腺激素通过 JNK 和 P38 MAPK 途径增强根尖乳头干细胞的牙向/成骨分化
DOI：
10.1155/2020/5128128
复制
发表时间：
2020-01-01
影响因子：
4.3
通讯作者：
Yu, Jinhua
中科院分区：
文献类型：
--
作者：
Pang, Xiyao;Zhuang, Ying;Yu, Jinhua
目的甲状旁腺激素(PTH)被认为是牙齿发育过程中必不可少的激素。来自顶端乳头的干细胞负责牙本质的形成。然而，甲状旁腺激素和SCAP之间的相互作用仍不清楚。本研究旨在探讨PTH对SCAPs成牙/成骨分化能力的影响，并阐明其分子机制。材料和方法在这里，SCAP是在体外分离和鉴定的。用细胞计数试剂盒(CCK-8)、流式细胞仪(FCM)和EDU检测PTH对SCAPs增殖的影响。碱性磷酸酶(ALP)活性、茜素红染色、Western印迹和RT-PCR检测PTH诱导的SCAPs成牙/成骨分化及MAPK信号转导途径的参与。结果碱性磷酸酶活力测定表明，10−8 /L甲状旁腺素是诱导SCAP的最佳浓度，CCK 8、FCM和EDU检测对SCAP的增殖无明显影响。成牙/成骨标志物的表达在mRNA水平和蛋白水平均显著上调。此外，间歇处理甲状旁腺素也增加了JNK和P38的磷酸化，抑制了JNK和P38的MAPK通路，抑制了分化。结论PTH可能通过JNK和P38MAPK途径调节SCAPs的成牙/成骨分化。
Objective Parathyroid hormone (PTH) is considered to be essential during the tooth development. Stem cells from the apical papilla (SCAPs) are responsible for dentine formation. However, the interaction between PTH and SCAPs remains unclear. This study was aimed at investigating the effects of PTH on odonto/osteogenic differentiation capacity of SCAPs and elucidating the underlying molecular mechanisms. Materials and Methods. Here, SCAPs were isolated and identified in vitro. Effects of PTH on the proliferation of SCAPs were determined by Cell Counting Kit-8 (CCK-8), flow cytometry (FCM), and EdU. Alkaline phosphatase (ALP) activity, alizarin red staining, Western blot, and RT-PCR were carried out to detect the odonto/osteogenic differentiation of PTH-treated SCAPs as well as the participation of the MAPK signaling pathway. Results An ALP activity assay determined that 10−8 mol/L PTH was the optimal concentration for the induction of SCAPs with no significant influence on the proliferation of SCAPs as indicated by CCK-8, FCM, and EdU. The expression of odonto/osteogenic markers was significantly upregulated in mRNA levels and protein levels. Moreover, intermittent treatment of PTH also increased phosphorylation of JNK and P38, and the differentiation was suppressed following the inhibition of JNK and P38 MAPK pathways. Conclusion PTH can regulate the odonto/osteogenic differentiation of SCAPs via JNK and P38 MAPK pathways.