Abstract
Pentraxin-3 (PTX3) is recognized as a modulator of inflammation and a mediator of tissue repair. In this study, we characterized the role of PTX3 on some biological functions of human dental pulp stem cells (HDPSCs). The expression level of PTX3 significantly increased during osteogenic/odontogenic differentiation of HDPSCs, whereas the knockdown of PTX3 decreased this differentiation. Silencing of PTX3 in HDPSCs inhibited their migration and C-X-C chemokine receptor type 4 (CXCR4) expression. Our present study indicates that PTX3 is involved in osteogenic/odontogenic differentiation and migration of HDPSCs, and may contribute to the therapeutic potential of HDPSCs for regeneration and repair.
Highlights
Until recently, inflammation in dental pulp was considered to exert only detrimental effects, but there is growing evidence regarding the consideration of the inflammatory process as a prerequisite for healing and regeneration in the dentin–pulp complex [1]
C-reactive protein (CRP) and serum amyloid P (SAP) are mainly expressed in hepatocytes in response to interleukin-6 (IL-6), whereas PTX3 is produced by different cell types at sites of local infection and inflammation [6]
We previously reported that PTX3 was inducible in human dental pulp cells upon stimulation with tumor necrosis factor-α (TNF-α) [8]; to our knowledge, the function of PTX3 in Human dental pulp stem cells (HDPSCs) has not been reported until now
Summary
Inflammation in dental pulp was considered to exert only detrimental effects, but there is growing evidence regarding the consideration of the inflammatory process as a prerequisite for healing and regeneration in the dentin–pulp complex [1]. Other studies hypothesized that dental pulp cells at the injured site were stimulated to express and secrete SDF-1, thereby activating CXCR4-positive HDPSCs and subsequently recruiting them toward the damaged site based on the SDF-1 gradient for reparative dentin formation [36,38]. We observed in this study that knockdown of PTX3 impaired the expression of CXCR4 and the cell migration ability of HDPSCs, indicating that PTX3 could affect the migration of HDPSCs toward SDF-1 Based on these observations, it is possible that the existence of CXCR4-positive HDPSCs with intact PTX3 and application of SDF-1 can increase the efficiency of biologically-based therapeutic approaches to regenerate or repair the dental pulp complex. This study may provide valuable clues regarding the development of HDPSC-mediated regenerative therapies, including dental pulp regeneration and repair
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