ArticleJournal of experimental zoology. Part B, Molecular and developmental evolution2009
Localization and function of the anion exchanger Ae2 in developing teeth and orofacial bone in rodents.
Article in Journal of experimental zoology. Part B, Molecular and developmental evolution, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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31 citing papers in PubMed, 42 citations in OpenAlex.
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- Exogenous transforming growth factor-β1 prevents the inflow of fluoride to ameleoblasts through regulation of voltage-gated chloride channels 5 and 7.Experimental and therapeutic medicine · 2021Article
- How pH is regulated during amelogenesis in dental fluorosis.Experimental and therapeutic medicine · 2018Review
- Importance of bicarbonate transport in pH control during amelogenesis - need for functional studies.Oral diseases · 2018Review
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- Mouse models of SLC4-linked disorders of HCOAmerican journal of physiology. Cell physiology · 2018Review
- Bicarbonate Transport During Enamel Maturation.Calcified tissue international · 2017Review
- Enamel: Molecular identity of its transepithelial ion transport system.Cell calcium · 2017Review
- DENTAL ENAMEL FORMATION AND IMPLICATIONS FOR ORAL HEALTH AND DISEASE.Physiological reviews · 2017Review
- Dose-Dependent Rescue of KO Amelogenin Enamel by TransgenesFrontiers in physiology · 2017Article
- Reduced Protein Expression of the NaCalcified tissue international · 2017Article
- Deletion ofFrontiers in physiology · 2017Article
- Null mutation of chloride channel 7 (Clcn7) impairs dental root formation but does not affect enamel mineralization.Cell and tissue research · 2016Article
- Ameloblast Modulation and Transport of Cl⁻, Na⁺, and K⁺ during Amelogenesis.Journal of dental research · 2015Article
- Amelogenins as potential buffers during secretory-stage amelogenesis.Journal of dental research · 2015Article
- Composition of mineralizing incisor enamel in cystic fibrosis transmembrane conductance regulator-deficient mice.European journal of oral sciences · 2015Article
- Article
- NBCe1 (SLC4A4) a potential pH regulator in enamel organ cells during enamel development in the mouse.Cell and tissue research · 2014Article
- Expression patterns and subcellular localization of carbonic anhydrases are developmentally regulated during tooth formation.PloS one · 2014Article
- The divergence, actions, roles, and relatives of sodium-coupled bicarbonate transporters.Physiological reviews · 2013Review
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9 authors at 5 institutions in 4 countries.
Funding
Abstract
To explore the functions of the anion exchanger 2 (Ae2) in the development of bones and teeth we examined the distribution of Ae2 in cells involved in the formation of teeth and surrounding bone in young hamsters, mice and rats. In all three species strongest immunostaining for Ae2 was obtained in basolateral membranes of maturation ameloblasts and in osteoclasts resorbing bone. In hamsters a weaker staining was also seen in the Golgi apparatus of secretory ameloblasts, young osteoblasts and osteocytes, odontoblasts and fibroblasts of the forming periodontal ligament. In adult Ae2(a,b) (-/-) mice, in which Ae2-targeted disruption precluded the expression of Ae2a, Ae2b1 and Ae2b2 isoforms, the immunostaining for Ae2 in ameloblasts and osteoclasts was totally abolished. The enamel formation was abnormal but teeth erupted, osteoclasts in jaw bone were functional and structure of dentin and bone was normal. In another mouse model, Ae2(-/-) mice in which the expression of all five Ae2 isoforms was disrupted, teeth failed to erupt and the alveolar bone proved poorly formed with giant but apparently functional osteoclasts. Our data indicate that basolaterally located Ae2a, Ae2b1 or Ae2b2 (or a combination of these) is present in maturation ameloblasts critical for the cells' normal functioning. Although isoforms of Ae2 were also present in basolateral membranes of osteoclasts, they proved to be not critical to osteoclast resorption of orofacial bone. Poorly formed bone and the failure of teeth to erupt seen in the Ae2(-/-) mice with gene disruption affecting all isoforms may result from secondary (systemic) changes that are different from Ae2(a,b) (-/-) mice.
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