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Developmental expression of solute carrier family 26A member 4 (SLC26A4/pendrin) during amelogenesis in developing rodent teeth
Author(s) -
Bronckers Antonius L. J. J.,
Guo Jing,
ZandiehDoulabi Behrouz,
Bervoets Theodore J.,
Lyaruu Donacian M.,
Li Xiangming,
Wangemann Philine,
DenBesten Pamela
Publication year - 2011
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/j.1600-0722.2011.00901.x
Subject(s) - ameloblast , amelogenesis , pendrin , cementoblast , chemistry , microbiology and biotechnology , apical membrane , immunostaining , enamel paint , odontoblast , enamel organ , endocrinology , anatomy , medicine , cementum , biology , dentin , membrane , pathology , biochemistry , dentistry , immunohistochemistry , transporter , gene
Bronckers ALJJ, Guo J, Zandieh‐Doulabi B, Bervoets TJ, Lyaruu DM, Li X, Wangemann P, DenBesten P. Developmental expression of solute carrier family 26A member 4 (SLC26A4/pendrin) during amelogenesis in developing rodent teeth.
Eur J Oral Sci 2011; 119 (Suppl. 1): 185–192. © 2011 Eur J Oral Sci Ameloblasts need to regulate pH during the formation of enamel crystals, a process that generates protons. Solute carrier family 26A member 4 (SLC26A4, or pendrin) is an anion exchanger for chloride, bicarbonate, iodine, and formate. It is expressed in apical membranes of ion‐transporting epithelia in kidney, inner ear, and thyroid where it regulates luminal pH and fluid transport. We hypothesized that maturation ameloblasts express SLC26A4 to neutralize acidification of enamel fluid in forming enamel. In rodents, secretory and maturation ameloblasts were immunopositive for SLC26A4. Staining was particularly strong in apical membranes of maturation ameloblasts facing forming enamel. RT‐PCR confirmed the presence of mRNA transcripts for Slc26a4 in enamel organs. SLC26A4 immunostaining was also found in mineralizing connective tissues, including odontoblasts, osteoblasts, osteocytes, osteoclasts, bone lining cells, cellular cementoblasts, and cementocytes. However , Slc26a4‐ null mutant mice had no overt dental phenotype. The presence of SLC26A4 in apical plasma membranes of maturation ameloblasts is consistent with a potential function as a pH regulator. SLC26A4 does not appear to be critical for ameloblast function and is probably compensated by other pH regulators.