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Sci Rep. 2015 Oct 30;5:15803. doi: 10.1038/srep15803.

Dental enamel cells express functional SOCE channels.

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Dept. Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, NY 10010, USA.
Dept. of Pathology, New York University School of Medicine, New York, NY 10016, USA.
Department of Anatomy &Cell Biology, McGill University, Facility for Electron Microscopy Research, Montreal, H3A 2B2, Canada.
Faculty of Dentistry, McGill University, Facility for Electron Microscopy Research, Montreal, H3A 2B2, Canada.
Dept. of Physiology, University of California, Los Angeles, 53-266 CHS, 10833 Le Conte Avenue, Los Angeles, California, USA.
Center for Craniofacial Molecular Biology, Ostrow School of Dentistry, University of Southern California, Los Angeles, California, CSA 135-HSC 9062, USA.
Departments of Paediatrics and Pharmacology, The University of Melbourne, Victoria 3010, Australia.


Dental enamel formation requires large quantities of Ca(2+) yet the mechanisms mediating Ca(2+) dynamics in enamel cells are unclear. Store-operated Ca(2+) entry (SOCE) channels are important Ca(2+) influx mechanisms in many cells. SOCE involves release of Ca(2+) from intracellular pools followed by Ca(2+) entry. The best-characterized SOCE channels are the Ca(2+) release-activated Ca(2+) (CRAC) channels. As patients with mutations in the CRAC channel genes STIM1 and ORAI1 show abnormal enamel mineralization, we hypothesized that CRAC channels might be an important Ca(2+) uptake mechanism in enamel cells. Investigating primary murine enamel cells, we found that key components of CRAC channels (ORAI1, ORAI2, ORAI3, STIM1, STIM2) were expressed and most abundant during the maturation stage of enamel development. Furthermore, inositol 1,4,5-trisphosphate receptor (IP3R) but not ryanodine receptor (RyR) expression was high in enamel cells suggesting that IP3Rs are the main ER Ca(2+) release mechanism. Passive depletion of ER Ca(2+) stores with thapsigargin resulted in a significant raise in [Ca(2+)]i consistent with SOCE. In cells pre-treated with the CRAC channel blocker Synta-66 Ca(2+) entry was significantly inhibited. These data demonstrate that enamel cells have SOCE mediated by CRAC channels and implicate them as a mechanism for Ca(2+) uptake in enamel formation.

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