Abstract

During tooth development, dental papilla cells differentiate into odontoblasts with polarized morphology and cell function. Our previous study indicated that the C-Jun N-terminal kinase (JNK) pathway regulates human dental papilla cell adhesion, migration, and formation of focal adhesion complexes. The aim of this study was to further examine the role of the JNK pathway in dental papilla cell polarity formation. Histological staining, qPCR, and Western Blot suggested the activation of JNK signaling in polarized mouse dental papilla tissue. After performing an in vitro tooth germ organ culture and cell culture, we found that JNK inhibitor SP600125 postponed tooth germ development and reduced the polarization, migration and differentiation of mouse dental papilla cells (mDPCs). Next, we screened up-regulated polarity-related genes during dental papilla development and mDPCs or A11 differentiation. We found that Prickle3, Golga2, Golga5, and RhoA were all up-regulated, which is consistent with JNK signaling activation. Further, constitutively active RhoA mutant (RhoA Q63L) partly rescued the inhibition of SP600125 on cell differentiation and polarity formation of mDPCs. To sum up, this study suggests that JNK signaling has a positive role in the formation of dental papilla cell polarization.

Highlights

  • At early stages, dental papilla cells appear small with a central nucleus and a few organelles

  • Those cells differentiate into preodontoblasts that are located along the basement membrane (BM), and polarizing odontoblasts, which are tall columnar with a polarized distribution of nuclear and cytoplasmic organelles [1, 2]

  • We further examined the role of the Jun N-terminal kinase (JNK) pathway in dental papilla cell polarity formation

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Summary

Introduction

Dental papilla cells appear small with a central nucleus and a few organelles. Those cells differentiate into preodontoblasts that are located along the basement membrane (BM), and polarizing odontoblasts, which are tall columnar with a polarized distribution of nuclear and cytoplasmic organelles [1, 2]. It is generally believed that the dental papilla cells and their polarization contributes to tooth formation, secretion of dentin, and pulp repair; yet, the molecular mechanism remains poorly understood. Only a few studies explored the molecular mechanism during the process of dental papilla cell polarization. Jimenez et al found that defective odontoblast.

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