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Am J Transl Res. 2019 Mar 15;11(3):1819-1826. eCollection 2019.

Loss of Wnt4 expression inhibits the odontogenic potential of dental pulp stem cells through JNK signaling in pulpitis.

Zhong TY1,2,3, Zhang ZC3, Gao YN1,2, Lu Z1,2, Qiao H1,2, Zhou H1,2, Liu Y1,3.

Author information

1
Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, Xi'an Jiaotong University Xi'an, Shaanxi, China.
2
Department of Orthodontics, The Affiliated Stomatological Hospital of Xi'an Jiaotong University Xi'an 710004, Shaanxi, China.
3
Institute of Neurobiology, Xi'an Jiaotong University Health Science Center Xi'an 710061, Shaanxi, China.

Abstract

Dental pulp stem cell (DPSC)-based odontogenic regeneration in inflammatory conditions is important in the process of pulpitis. DPSCs have been reported to lose potential for odontogenic regeneration in inflammatory conditions. This study aims to determine the mechanism of impaired odontogenic differentiation of DPSCs in an inflammatory microenvironment. We regulated Wnt4 expression using recombinant lentiviral Wnt4 and Wnt4 siRNA. Alkaline phosphatase (ALP) and Alizarin red S (ARS) staining as well as Real-Time PCR were performed to evaluate the osteogenic differentiation potential of DPSCs with either upregulated or downregulated Wnt4. Furthermore, SP600125 was used to inhibit the potential downstream factor JNK1, and the osteogenic differentiation ability of DPSCs was evaluated. As shown, Wnt4 was downregulated in DPSCs under inflammatory conditions. Inhibition of Wnt4 expression in DPSCs negatively regulated odontogenic differentiation. Overexpression of Wnt4 in LPS-treated DPSCs promoted odontogenic differentiation. In addition, JNK1 was responsible for Wnt4-mediated odontogenic differentiation of DPSCs. Taken together, Wnt4 may function by affecting JNK signaling pathways in the process of impaired odontogenic regeneration by DPSCs under inflammatory conditions.

KEYWORDS:

Dental pulp stem cells; Wnt4; inflammatory; microenvironment

PMID:
30972205
PMCID:
PMC6456534

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