(The FASEB Journal. 2007;21:916.9)
© 2007 FASEB
Expression of AE2 and NBC1 in Secretory Ameloblasts
Michael Paine1,
HongJun Wang1,
Natalia Abuladze2,
Weixin Liu2,
Susan M. Wall3,
Young-Hee Kim3 and
Ira Kurtz2
1 School of Dentistry, USC, 2250 Alcazar St, Los Angeles, CA, 90033,
2 Medicine, UCLA, 10833 Le Conte AAve, Los Angeles, CA, 90095,
3 Medicine, Emory University, 1639 Pierce Dr, Atlanta, GA, 30322
ABSTRACT
Tooth enamel is a product of ectoderm-derived cells called ameloblasts, and in its final form enamel is a reflection of the unique molecular and cellular activities characteristic of amelogenesis. In the rodent model enamel formation (amelogenesis) occurs rapidly with approximately 100 µm of enamel thickness being formed in days. For this process to proceed normally, the pH of the microenvironment adjacent to the ameloblast must be regulated properly during apatite deposition and crystallite growth. Animal models null for the AE2 anion exchanger have abnormal enamel. Similarly, patients with mutations in the sodium bicarbonate cotransporter NBC1 (NBCe1) have dental enamel defects. Both these observations suggest roles for AE2 and NBC1 in amelogenesis. This study was done to define the distribution of AE2 and NBC1 in polar, secretory ameloblast cells in both molar and incisor teeth. We show that NBC1 is expressed at the basal pole, and that AE1 is expressed at the apical pole of secretory ameloblast cells. RT-PCR, using RNA isolated from using cultured ameloblast-like LS8 cells, was able to confirm the presence of mRNA transcripts for AE2 and NBC1. In these cells the transcripts for AE2a and pNBC1 (NBCe1-B) were highly expressed. Our data show the location of AE2 and NBC1 in ameloblast cells in vivo, thus indicating a functional role for AE2 and NBC1 during amelogenesis. Mutations in either protein result in abnormal enamel production and confirm the significant role of bicarbonate transport to the formation of enamel.
