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Osteolectin Promotes Odontoblastic Differentiation in Human Dental Pulp Cells. | LitMetric

Osteolectin Promotes Odontoblastic Differentiation in Human Dental Pulp Cells.

J Endod

Department of Conservative Dentistry, School of Dentistry, Dental Science Research Institute, Chonnam National University, Gwangju, Republic of Korea. Electronic address:

Published: December 2023

AI Article Synopsis

  • Osteolectin, a secreted glycoprotein found in bone tissues, is identified as a new factor that enhances bone regeneration and its effects on human dental pulp cells (hDPCs) were explored for the first time.
  • Experimental methods revealed that osteolectin is noncytotoxic at concentrations below 300 ng/ml and significantly promotes odontoblastic differentiation through increased alkaline phosphatase (ALP) activity and mineralization, as well as up-regulation of specific genes and proteins.
  • The signaling mechanisms involved include the activation of key pathways (ERK, JNK, and AKT), and blocking these pathways resulted in reduced differentiation and mineralization activities in hDPCs.

Article Abstract

Introduction: Osteolectin is a secreted glycoprotein of the C-type lectin domain superfamily, expressed in bone tissues and is reported as a novel osteogenic factor that promotes bone regeneration. However, the effect of osteolectin on human dental pulp cells (hDPCs) has not been reported. Therefore, we aimed to investigate the odontoblastic differentiation of osteolectin in hDPCs and further attempt to reveal its underlying mechanism.

Methods: Cytotoxicity assays were used to detect the cytotoxicity of osteolectin. The odontoblastic differentiation of hDPCs and its underlying mechanisms were measured by the alkaline phosphatase (ALP) activity, mineralized spots formation, and the gene and protein expression of odontoblastic differentiation through ALP staining, Alizarin red S staining, quantitative real-time polymerase chain reaction, and Western blot analysis, respectively.

Results: WST-1 assay showed osteolectin at concentrations below 300 ng/ml was noncytotoxic and safe for hDPCs. The following experiment demonstrated that osteolectin could increase ALP activity, accelerate the mineralization process, and up-regulate the odontogenic differentiation markers in both gene and protein levels (P < .05). Osteolectin stimulated the phosphorylation of ERK, JNK, and Protein kinase B (AKT) in hDPCs. Extracellular signal-regulated kinase (ERK), Jun N-terminal kinase (JNK), and AKT inhibitors decreased ALP activity and mineralization capacity and suppressed the expression of dentin sialophosphoprotein and dentin matrix protein-1.

Conclusion: Osteolectin can promote odontoblastic differentiation of hDPCs, and the whole process may stimulate ERK, JNK, and AKT signaling pathways by increasing p-ERK, p-JNK, and p-AKT signals.

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Source
http://dx.doi.org/10.1016/j.joen.2023.09.010DOI Listing

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