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The Activin-binding Protein Follistatin is Expressed in Developing Murine Molar and Induces Odontoblast-like Cell Differentiation in vitro

Institut de Biologie Medicale, Université Louis Pasteur, Faculte de Medecine, INSERM U 424, Strasbourg, France, Institute of Dentistry, University of Turku, FIN-20520 Turku, Finland

C. Begue-Kirn

Institut de Biologie Medicale, Université Louis Pasteur, Faculte de Medecine, INSERM U 424, Strasbourg, France

O. Ritvos

University of Helsinki, Haartman Institute, Department of Bacteriology and Immunology, FIN-00014 Helsinki, Finland

T. Tuuri

University of Helsinki, Haartman Institute, Department of Bacteriology and Immunology, FIN-00014 Helsinki, Finland

J.V. Ruch

Institut de Biologie Medicale, Université Louis Pasteur, Faculte de Medecine, INSERM U 424, Strasbourg, France

It has recently been shown that mice deficient in activin-βA subunits and follistatin exhibit major defects in dentition. To increase understanding of the roles played by these molecules during tooth development, we determined the temporospatial expression of activin-βA subunit and follistatin messenger RNA and their corresponding proteins in developing murine molars (between day E 14 and 2 days after birth). The effects of recombinant human activin A and its binding protein follistatin on odontoblast differentiation were also studied in cultures of dental papillae (DP) isolated from the mandibular first molars of E-17-day mice. In situ hybridization indicated that transcripts for activin-βA subunit were abundant in pre-odontoblasts at the tips of forming cusps prior to odontoblast terminal differentiation, and transcripts for follistatin in overlying inner enamel epithelial cells (pre-ameloblasts). Pre-odontoblasts were also weakly immunoreactive in relation to activin-βA subunit, pre-ameloblasts in relation to follistatin. When follistatin was added at different concentrations to a DP culture model (2-14 nmol/DP) together with heparin at constant concentration, differentiation of odontoblast-like cells was induced, as evidenced by polarization and deposition of extracellular matrix in vitro, to extents depending on the follistatin concentration. In contrast, the addition of activin A (2 nmol/DP) had no effect on the differentiation parameters studied. These findings suggest that the activin-follistatin system regulates odontoblast differentiation during tooth development. In particular, we suggest that binding of endogenous activin A by follistatin may allow odontoblast terminal differentiation to occur.

Key Words: activin A • follistatin • immunohistochemistry • in situ hybridization • odontoblasts • dental papilla culture.

Journal of Dental Research, Vol. 76, No. 10, 1625-1636 (1997)
DOI: 10.1177/00220345970760100301


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