All ETDs from UAB

Advisory Committee Chair

Ping Zhang

Advisory Committee Members

Janice G Jackson

Amjad Javed

Noel Childers

Kimberly Carr

Document Type


Date of Award


Degree Name by School

Master of Science (MS) School of Dentistry


Purpose: Dentin is produced from odontoblasts, derived from human Dental Pulp Cells (hDPCs), which are essential for dentin formation, remodeling, and mineral hemostasis. Epigenetic mechanisms are believed to be involved in odontoblast differentiation and function, and H3K4 methylation is associated with gene activation which is fundamental to histone-based epigenetics. The SET1/MLL complexes are mammals' major histone H3K4 methylation enzymes. DPY30 is a core subunit of SET1/MII complexes, mammalian's major histone H3K4 methyltransferases. It plays an important role in regulating fundamental processes including the determination of cell lineage, growth, and differentiation. Thus, histone-based epigenetic mechanisms are involved in odontoblast differentiation and function. Objective: To determine the role of DPY30 in the epigenetic regulation of odontoblast differentiation and mineralization in vitro. Methods: Primary human dental pulp cells (hDPCs) were used to induce odontoblast differentiation. Odontoblast differentiation and mineralization were determined by alkaline phosphate (ALP) staining, and alizarin red (ARS) staining, respectively. The expression of DPY30 and odontoblast-related genes were assessed on days 0, 3, 7, 14, and 21 of differentiation by quantitative PCR. The siRNA knockdown of DPY30 was used to determine the effect of DPY30 on odontoblast differentiation and mineralization. The role of DPY30 in the regulation of odontoblast-related gene expression was also assessed. Results: During hDPCs differentiation, the expression of DPY30 increased from day 3 to day 21, along with a progressive increase in the expression of both early (RUNX2, COL1α, DSPP) and late (DMP1, OCN) marker genes. Differentiation of hDPCs to odontoblasts was further confirmed by ALP and ARS staining. Successful knockdown of DPY30 was achieved and confirmed by qPCR. DPY30 knockdown in hDPCs led to a marked reduction in ALP activity and odontoblast differentiation. In addition, the expression of odontogenic marker genes RUNX2, COL1α, DSPP, DMP1, and OCN was significantly reduced by DPY30 depletion. Conclusion: Our results demonstrate the crucial role of DPY30 in the regulation of odontogenic differentiation and mineralization of hDPCs in vitro. Therefore, it may be possible to develop epigenetic-based remedies for genetic disorders that affect dentin development by understanding the role of histone modifications during odontoblast differentiation.

Included in

Dentistry Commons



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