Abstract
Human dental pulp cells (hDPCs) have shown their plasticity when treated with the hydroxamate-based histone deacetylase (HDAC) inhibitor members, Trichostatin A (TSA), and suberoylanilide hydroxamic acid (SAHA). However, a comparison of their potency to stimulate odontoblast-like differentiation and mineralization has not been reported. The aim of our study was to confirm and compare these TSA and SAHA effects. Primary hDPCs cultured with/without various TSA or SAHA concentrations were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), ALP activity, alizarin red staining, and scratch wound healing assays. The inhibitory effect of TSA and SAHA on inhibiting the activity of HDAC was evaluated by HDAC activity assay. Odontoblast-related gene expression was determined using RT-qPCR. The MTT assay indicated that TSA or SAHA did not affect hDPC viability. TSA or SAHA treatment-induced odontoblast-like differentiation as evidenced by a significant increase in alkaline phosphatase activity and mineral deposition after 400 nM TSA or 1 μM SAHA treatment. A significant increase in nuclear factor I C, kruppel like factor 4, dentin matrix acidic phosphoprotein 1, dentin sialophosphoprotein, collagen type I alpha 1 chain, alkaline phosphatase (ALPL), integrin-binding sialoprotein, bone gamma-carboxyglutamate protein, vascular endothelial growth factor A, and cyclin-dependent kinase inhibitor 1A gene expression analyzed by RT-qPCR, at 24, 72 h, 7, and 10 days of treatment. The activity of HDAC in hDPCs culture was significantly inhibited after 72 h TSA and SAHA treatment. The scratch wound healing assay displayed enhanced cell migration at 72 h after TSA or SAHA treatment. Our findings demonstrated that TSA and SAHA have similar stimulatory effects in inducing HDPC odontogenic differentiation and mineralization and propose another potential use of TSA and SAHA to promote dentin regeneration.
Highlights
The breakdown of the dentine layer triggered by a deep dental cavity commonly leads to dental pulp inflammation [1], and a pulp-capping material may be required to stimulate reparative dentine formation and protect the pulp tissue from further inflammation
To evaluate the effect of Trichostatin A (TSA) and suberoylanilide hydroxamic acid (SAHA) treatment on Human dental pulp cells (hDPCs) viability, an MTT assay was performed in an osteogenic medium containing 50, 200, 400 nM, or 800 nM TSA; or 0.5, 1, 3, 5, or 10 μM SAHA for 72 h
At 72 h posttreatment, hDPC viability was not influenced by 50 nM, 200 nM, or 400 nM TSA; or 0.5 and 1 μM SAHA treatment compared with the control
Summary
The breakdown of the dentine layer triggered by a deep dental cavity commonly leads to dental pulp inflammation (pulpitis) [1], and a pulp-capping material may be required to stimulate reparative dentine formation and protect the pulp tissue from further inflammation. Dental pulp cells can differentiate into odontoblast-like cells and generate reparative dentine formation in response to damaged dentine. This ability indicates that pulp tissue contains odontogenic progenitor or stem cells that can differentiate into multiple cell lineages, including odontoblasts, osteoblasts, and adipocytes [14, 15]. Every cell in an individual carries the same genetic information encoded in their chromosomes [16] Their exposure to specific signaling molecules are essential to control the cell fate decision, proliferation, and differentiation involved in reparative dentin formation [3, 15, 17, 18]
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