Pentraxin-3 Promotes Inflammatory Response in Human Dental Pulp Cells

Objectives: Pentraxin-3 produced by a variety of tissues in response to proinflammatory signals has shown to be involved in inflammatory responses. The aims of this study were to explore the role of pentraxin-3 in dental pulp inflammation in human dental pulp cells (HDPCs).
Methods: HDPCs were treated with TNF-α or pentraxin-3, and total RNA or proteins were extracted and analyzed by reverse transcription polymerase chain reaction or western blotting. For knockdown of pentraxin-3, HDPCs were transfected with siRNA against human pentraxin-3. Expressional pattern of pentraxin-3 in inflamed pulp tissues was assessed by immunohistochemical staining.
Results: In the present study, we found that TNF-α increases the levels of mRNA and protein of pentraxin-3 in HDPCs. TNF-α-induced pentraxin-3 expression is mediated by p38MAPK, ERK, AKT-dependent and NF-κB-dependent manner. The knockdown of pentraxin-3 decreased the expression levels of IL-6, IL-8, and MCP-1 after stimulation with TNF-α in HDPCs. The treatment of pentraxin-3 further increased the expression of cytokines including IL-6, IL-8, and MCP-1. Moreover, immunohistochemical analysis showed pentraxin-3 is highly expressed in inflamed pulp tissues.
Conclusions: Taken together, our findings indicated a critical role for pentraxin-3 in regulating dental inflammatory processes and revealed its underlying molecular mechanism.