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@ARTICLE{Bardet:276851,
author = {Bardet, Claire and Courson, Frédéric and Wu, Yong and
Khaddam, Mayssam and Salmon, Benjamin and Ribes, Sandy and
Thumfart, Julia and Yamaguti, Paulo M and Rochefort, Gael Y
and Figueres, Marie-Lucile and Breiderhoff, Tilman and
Garcia-Castaño, Alejandro and Vallée, Benoit and Le
Denmat, Dominique and Baroukh, Brigitte and Guilbert, Thomas
and Schmitt, Alain and Massé, Jean-Marc and Bazin,
Dominique and Lorenz, Georg and Morawietz, Maria and Hou,
Jianghui and Carvalho-Lobato, Patricia and Manzanares, Maria
Cristina and Fricain, Jean-Christophe and Talmud, Deborah
and Demontis, Renato and Neves, Francisco and Zenaty,
Delphine and Berdal, Ariane and Kiesow, Andreas and Petzold,
Matthias and Menashi, Suzanne and Linglart, Agnes and
Acevedo, Ana Carolina and Vargas-Poussou, Rosa and Müller,
Dominik and Houillier, Pascal and Chaussain, Catherine},
title = {{C}laudin-16 {D}eficiency {I}mpairs {T}ight {J}unction
{F}unction in {A}meloblasts, {L}eading to {A}bnormal
{E}namel {F}ormation.},
journal = {Journal of bone and mineral research},
volume = {31},
number = {3},
issn = {0884-0431},
address = {[Oxford]},
publisher = {Oxford University Press},
reportid = {DZNE-2025-00364},
pages = {498 - 513},
year = {2016},
abstract = {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.},
keywords = {Adult / Ameloblasts: metabolism / Ameloblasts: pathology /
Amelogenesis Imperfecta: metabolism / Amelogenesis
Imperfecta: pathology / Animals / Child / Claudins:
deficiency / Claudins: genetics / Dental Enamel:
abnormalities / Dental Enamel: metabolism / Dental Enamel:
pathology / Female / Humans / Hydrogen-Ion Concentration /
Male / Mice / Middle Aged / Mutation: genetics / Phenotype /
Syndrome / Tight Junctions: metabolism / Young Adult /
AMELOGENESIS IMPERFECTA (AI) (Other) / FAMILIAL
HYPOMAGNESEMIA WITH HYPERCALCIURIA AND NEPHROCALCINOSIS
(FHHNC) (Other) / MMP-20 (Other) / SECRETORY AMELOBLASTS
(Other) / pH (Other) / Claudins (NLM Chemicals) / claudin 16
(NLM Chemicals)},
ddc = {610},
pnm = {899 - ohne Topic (POF4-899)},
pid = {G:(DE-HGF)POF4-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:26426912},
doi = {10.1002/jbmr.2726},
url = {https://pub.dzne.de/record/276851},
}