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Cementum protein 1 (CEMP1) activates p38 and JNK during the mineralisation process by cementoblast-like cells in vitro


Abstract:
We recently presented evidence showing that cementum protein 1 (CEMP1) promotes periodontal ligament (PDL) cell migration, proliferation, expression of bone, and cementum-matrix proteins and mineralisation. In other words, it induces PDL precursor cells commitment toward a cementoblast-like cells phenotype. The intracellular signalling pathways involved in cementoblast differentiation and mineralisation have not been well characterised. JNK and p38 protein kinases (MAPKs) are intracellular signalling pathways and key mediators of cellular processes such as proliferation and differentiation. Since signalling pathways involving MAPKs have been associated with osteoblastic phenotype, in this study we investigated the effect of hrCEMP1 and mineralising media containing β-glycerophosphate and ascorbic acid on the activation of p38-MAPK and JNK–MAPK in cementoblast-like cells. Our results show that mineralising media and hrCEMP1 induced phosphorylation of p38 and JNK kinases. Mineralising media containing hrCEMP1 increased the activation of p38-MAPK and its translocation to the cell nucleus; increased phosphorylation of JNK–MAPK and induced the phosphorylation of the protein C-JUN. We also demonstrate that hrCEMP1 regulates the expression of BSP, OCN, and ALP specific activity. We found that hrCEMP1 and mineralising media promote nodule formation. These findings give an insight into the signalling pathways activated by hrCEMP1 and suggest likely components of the mechanisms that regulate the formation and regeneration of cementum and surrounding connective tissues.

Keywords:
cell signalling pathways; cementoblasts; CEMP; MAPK; mineralisation


Autoři: Silvia Maldonado 1;  Enrique Romo 1;  Janeth Serrano 1;  Adriana Perez 1;  Christian Guerra 2;  Margarita Zeichner-David 3;  Gabriela Mercado 1;  Higinio Arzate 1*
Působiště autorů: Laboratorio de Biología Periodontal, Facultad de Odontología, Universidad Nacional Autónoma de Mexico, Mexico, D. F., Mexico 1;  Unidad de Investigación Medica en Farmacología, Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Mexico, D. F., Mexico 2;  Ostrow School of Dentistry of the University of Southern California, Los Angeles, California, USA 3
Vyšlo v časopise: Cell Biology International Reports, 21, 2014, č. 1, s. 8-16
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1002/cbi3.10011

© 2014 The Authors. Cell Biology International Reports published by John Wiley & Sons Ltd on behalf of the International Federation for Cell Biology.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Cell Biol Int Rep 21 (2014) 17–24  2014 The Authors. Cell Biology International Reports published by John Wiley & Sons Ltd on behalf of the International Federation for Cell Biology.

Souhrn

Abstract:
We recently presented evidence showing that cementum protein 1 (CEMP1) promotes periodontal ligament (PDL) cell migration, proliferation, expression of bone, and cementum-matrix proteins and mineralisation. In other words, it induces PDL precursor cells commitment toward a cementoblast-like cells phenotype. The intracellular signalling pathways involved in cementoblast differentiation and mineralisation have not been well characterised. JNK and p38 protein kinases (MAPKs) are intracellular signalling pathways and key mediators of cellular processes such as proliferation and differentiation. Since signalling pathways involving MAPKs have been associated with osteoblastic phenotype, in this study we investigated the effect of hrCEMP1 and mineralising media containing β-glycerophosphate and ascorbic acid on the activation of p38-MAPK and JNK–MAPK in cementoblast-like cells. Our results show that mineralising media and hrCEMP1 induced phosphorylation of p38 and JNK kinases. Mineralising media containing hrCEMP1 increased the activation of p38-MAPK and its translocation to the cell nucleus; increased phosphorylation of JNK–MAPK and induced the phosphorylation of the protein C-JUN. We also demonstrate that hrCEMP1 regulates the expression of BSP, OCN, and ALP specific activity. We found that hrCEMP1 and mineralising media promote nodule formation. These findings give an insight into the signalling pathways activated by hrCEMP1 and suggest likely components of the mechanisms that regulate the formation and regeneration of cementum and surrounding connective tissues.

Keywords:
cell signalling pathways; cementoblasts; CEMP; MAPK; mineralisation


Zdroje

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