Claudin-16 Deficiency Impairs Tight Junction Function in Ameloblasts, Leading to Abnormal Enamel Formation - Sorbonne Université
Article Dans Une Revue Journal of Bone and Mineral Research Année : 2015

Claudin-16 Deficiency Impairs Tight Junction Function in Ameloblasts, Leading to Abnormal Enamel Formation

Julia Thumfart
  • Fonction : Auteur
Paulo M Yamaguti
  • Fonction : Auteur
Tilman Breiderhoff
  • Fonction : Auteur
Alejandro Garcia-Castaño
  • Fonction : Auteur
Thomas Guilbert
Alain Schmitt
  • Fonction : Auteur
Jean-Marc Massé
  • Fonction : Auteur
Georg Lorenz
  • Fonction : Auteur
Maria Morawietz
  • Fonction : Auteur
Jianghui Hou
  • Fonction : Auteur
Patricia Carvalho-Lobato
  • Fonction : Auteur
Maria Cristina Manzanares
  • Fonction : Auteur
Francisco Neves
  • Fonction : Auteur
Andreas Kiesow
  • Fonction : Auteur
Matthias Petzold
  • Fonction : Auteur
Agnes Linglart
Ana Carolina Acevedo
  • Fonction : Auteur
Rosa Vargas-Poussou

Résumé

Claudin-16 protein (CLDN16) is a component of tight junctions (TJ) with a restrictive distribution so far demonstrated mainly in the kidney. Here, we demonstrate the expression of CLDN16 also in the tooth germ and show that claudin-16 gene (CLDN16) mutations result in amelogenesis imperfecta (AI) in the 5 studied patients with familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC). To investigate the role of CLDN16 in tooth formation, we studied a murine model of FHHNC and showed that CLDN16 deficiency led to altered secretory ameloblast TJ structure, lowering of extracellular pH in the forming enamel matrix, and abnormal enamel matrix protein processing, resulting in an enamel phenotype closely resembling human AI. This study unravels an association of FHHNC owing to CLDN16 mutations with AI, which is directly related to the loss of function of CLDN16 during amelogenesis. Overall, this study indicates for the first time the importance of a TJ protein in tooth formation and underlines the need to establish a specific dental follow-up for these patients. © 2015 American Society for Bone and Mineral Research.

Dates et versions

hal-01286223 , version 1 (10-03-2016)

Identifiants

Citer

Claire Bardet, Frédéric Courson, Yong Wu, Mayssam Khaddam, Benjamin Salmon, et al.. Claudin-16 Deficiency Impairs Tight Junction Function in Ameloblasts, Leading to Abnormal Enamel Formation. Journal of Bone and Mineral Research, 2015, 31 (3), pp.498-513. ⟨10.1002/jbmr.2726⟩. ⟨hal-01286223⟩
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