Testicular acid phosphatase induces odontoblast differentiation and mineralization
Autor: | Eui-Sic Cho, Hwajung Choi, Tak-Heun Kim, Jung-Wook Kim, Chi-Young Yun |
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Rok vydání: | 2015 |
Předmět: |
Male
0301 basic medicine Pathology medicine.medical_specialty Histology Mesenchyme Acid Phosphatase Odontoblast differentiation Biology Gene Expression Regulation Enzymologic Cell Line Pathology and Forensic Medicine Mice 03 medical and health sciences Calcification Physiologic 0302 clinical medicine Cyclin D1 stomatognathic system medicine Animals Odontoblasts Cell growth PHEX Acid phosphatase Cell Differentiation 030206 dentistry Cell Biology Antigens Differentiation Cell biology 030104 developmental biology Odontoblast medicine.anatomical_structure Gene Knockdown Techniques biology.protein Alkaline phosphatase |
Zdroj: | Cell and Tissue Research. 364:95-103 |
ISSN: | 1432-0878 0302-766X |
Popis: | Odontoblasts differentiate from dental mesenchyme during dentin formation and mineralization. However, the molecular mechanisms controlling odontoblast differentiation remain poorly understood. Here, we show that expression of testicular acid phosphatase (ACPT) is restricted in the early stage of odontoblast differentiation in proliferating dental mesenchymal cells and secretory odontoblasts. ACPT is expressed earlier than tissue-nonspecific alkaline phosphatase (TNAP) and partly overlaps with TNAP in differentiating odontoblasts. In MDPC-23 odontoblastic cells, expression of ACPT appears simultaneously with a decrease in β-catenin activity and is abolished with the expression of Phex and Dsp. Knockdown of ACPT in MDPC-23 cells stimulates cell proliferation together with an increase in active β-catenin and cyclin D1. In contrast, the overexpression of ACPT suppresses cell proliferation with a decrease in active β-catenin and cyclin D1. Expression of TNAP, Osx, Phex and Dsp is reduced by knockdown of ACPT but is enhanced by ACPT overexpression. When ACPT is blocked with IgG, alkaline phosphatase activity is inhibited but cell proliferation is unchanged regardless of ACPT expression. These findings suggest that ACPT inhibits cell proliferation through β-catenin-mediated signaling in dental mesenchyme but elicits odontoblast differentiation and mineralization by supplying phosphate during dentin formation. Thus, ACPT might be a novel candidate for inducing odontoblast differentiation and mineralization for dentin regeneration. |
Databáze: | OpenAIRE |
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