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RESEARCH REPORT |
1 University of Southern California, School of Dentistry, Center for Craniofacial Molecular Biology, 2250 Alcazar Street, CSA Room 103, Los Angeles, CA 90033, USA;
2 David Geffen School of Medicine at UCLA, 10833 Le Conte Ave., Los Angeles, CA 90095, USA; and
3 Department of Medicine, Emory University, 1639 Pierce Dr., Atlanta, GA 30322, USA
* corresponding author, UCLA Division of Nephrology, 10833 Le Conte Avenue, Room 7-155 Factor Building, Los Angeles, CA 90095-1689, USA; ikurtz{at}mednet.ucla.edu
The H+/base transport processes that control the pH of the microenvironment adjacent to ameloblasts are not currently well-understood. Mice null for the AE2 anion exchanger have abnormal enamel. In addition, persons with mutations in the electrogenic sodium bicarbonate co-transporter NBCe1 and mice lacking NBCe1 have enamel abnormalities. These observations suggest that AE2 and NBCe1 play important roles in amelogenesis. In the present study, we aimed to understand the roles of AE2 and NBCe1 in ameloblasts. Analysis of the data showed that NBCe1 is expressed at the basolateral membrane of secretory ameloblasts, whereas AE2 is expressed at the apical membrane. Transcripts for AE2a and NBCe1-B were detected in RNA isolated from cultured ameloblast-like LS8 cells. Our data are the first evidence that AE2 and NBCe1 are expressed in ameloblasts in vivo in a polarized fashion, thereby providing a mechanism for ameloblast transcellular bicarbonate secretion in the process of enamel formation and maturation.
KEY WORDS: amelogenesis • anion exchanger • enamel • sodium bicarbonate co-transporter
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| IADR Journals | Advances in Dental Research ® |
| Journal of Dental Research ® | Critical Reviews (1990-2004) |
