Intermittent Administration of Parathyroid Hormone Enhances Odonto/Osteogenic Differentiation of Stem Cells from the Apical Papilla via JNK and P38 MAPK Pathways.

Xiyao Pang,Changao Xue,Qin Cai,Ying Zhuang,Fengge Zhang,Zehan Li,Shuanglin Jing,Jinhua Yu

doi:10.1155/2020/5128128

Abstract

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.

Highlights

Dental pulp, a mineralized connective tissue, has the intrinsic ability to form reparative dentine when insulted due to trauma or infection [1, 2]
flow cytometry (FCM) findings revealed that these cells were positive for CD29, CD105, CD90, and CD73 while negative for CD34 and CD45
extracellular signal-regulated kinase (ERK) responded negatively to the intermittent administration of Parathyroid hormone (PTH) in a time-dependent manner, which means that ERK is not activated (Figures 4(a) and 4(d), P < 0:05). These results suggest that intermittent PTH treatment increases phosphorylation of Jun N-terminal kinase (JNK) and P38

Summary

Introduction

A mineralized connective tissue, has the intrinsic ability to form reparative dentine when insulted due to trauma or infection [1, 2]. Stem cell populations and biomaterials are verified for dental pulp tissue regeneration. SCAPs reside in the root apex of incompletely developed teeth which can be isolated [3]. The role of SCAPs during root formation is observed in many studies [5]. In vivo studies showed that root development can be halted when cells were isolated from tooth buds at an early stage [6]. The easy accessibility and superior properties established them as an attractive choice for tooth and bone tissue engineering

Methods

Results

Conclusion