Zdhhc8 Expression In Odontogenic Differentiation Of Human Dental Pulp Cells
Human dental pulp cells (hDPCs) can generate reparative dentin specifically under external stimuli, and protein S-palmitoylation is involved in this process. ZDHHC8 is a palmitoyl acyltransferase that plays a significant role in cell proliferation and differentiation. However, the specific role of ZDHHC8 in hDPCs odontogenic differentiation is still unknown. hDPCs were obtained from extracted healthy third molars and premolars approved by the Ethical Review Board. Cells of passage 3-5 were cultured in the odontogenic differentiation medium or growth medium for different days. On day 7 and day 14, ALP staining was performed. On day 14 alizarin red staining was performed. On days 0, 7, 14 and 21 the mRNA expression of DSPP, RUNX2 and ALP was evaluated utilizing real-time quantitative polymerase chain reaction (qRT-PCR) to detect the ability of odontogenic differentiation. The potential changes of ZDHHC8 mRNA level were measured by qRT-PCR. Protein expression of ZDHHC8 was assessed using Western Blot. ALP, ARS, and qRT-PCR showed that hDPCs were successfully induced. ZDHHC8 presented in hDPCs. During odontogenic differentiation, the ZDHHC8 mRNA and protein expression levels in the hDPCs were increased on days 7, 14 and 21. This level reached a peak on day 14 and decreased on day 21. The expression level of palmitoyl acyltransferase ZDHHC8 enhanced during hDPCs odontogenic differentiation. ZDHHC8 may be associated with the regulation of dental pulp cell differentiation.
Authors
- Luyuan Chen (ORCID: https://orcid.org/0000-0003-3506-5296)
- Baicheng Yi
- Xinxuan Wang
- Zhihui Chen (ORCID: https://orcid.org/0009-0008-3959-9483)
Institutions
- University of Hong Kong - Shenzhen Hospital (CN)
- Southern Medical University Shenzhen Hospital (CN)
Publication Details
- Journal
- International Dental Journal
- Published
- 2025-10-01
- DOI
- https://doi.org/10.1016/j.identj.2025.104408
- Primary Topic
- Bone and Dental Protein Studies
- Type
- article
- Field-Weighted Citation Impact
- 0.00