Incisor enamel formation is impaired in transgenic rats overexpressing the type III NaPi transporter Slc20a1

Hirotaka Yoshioka, Yuji Yoshiko, Tomoko Minamizaki, Sayaka Suzuki, Yoshiro Koma, Asako Nobukiyo, Yusuke Sotomaru, Atsushi Suzuki, Mitsuyasu Itoh, Norihiko Maeda

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Inorganic phosphate (Pi) is required in many biological processes, including signaling cascades, skeletal development, tooth mineralization, and nucleic acid synthesis. Recently, we showed that Pi transport in osteoblasts, mediated by Slc20a1, a member of the type III sodium-dependent phosphate transporter family, is indispensable for osteoid mineralization in rapidly growing rat bone. In addition, we found that bone mineral density decreased slightly with dysfunction of Pi homeostasis in aged transgenic rats overexpressing mouse Slc20a1 (Slc20a1-Tg). Bone and tooth share certain common molecular features, and thus, we focused on tooth development in Slc20a1-Tg mandibular incisors in order to determine the role of Slc20a1 in tooth mineralization. Around the time of weaning, there were no significant differences in serologic parameters between wild-type and Slc20a1-Tg rats. However, histological analysis showed that Slc20a1-Tg ameloblasts formed clusters in the papillary layer during the maturation stage as early as 4 weeks of age. These pathologies became more severe with age and included the formation of cyst-like or multilayer ameloblast structures, accompanied by a chalky white appearance with abnormal attrition and fracture. Hyperphosphatemia was also observed in aging Slc20a1-Tg rats. Micro-computed tomography and electron probe microanalysis revealed impairments in enamel, such as delayed mineralization and hypomineralization. Our results suggest that enamel formation is sensitive to imbalances in Pit1-mediated cellular function as seen in bone, although these processes are under the control of systemic Pi homeostasis.

Original languageEnglish
Pages (from-to)192-202
Number of pages11
JournalCalcified Tissue International
Volume89
Issue number3
DOIs
Publication statusPublished - 01-09-2011

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Transgenic Rats
Incisor
Dental Enamel
Tooth
Ameloblasts
Bone and Bones
Homeostasis
Sodium-Phosphate Cotransporter Proteins
Hyperphosphatemia
Biological Phenomena
Electron Probe Microanalysis
Weaning
Osteoblasts
Bone Density
Nucleic Acids
Cysts
Phosphates
Tomography
Pathology

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Orthopedics and Sports Medicine
  • Endocrinology

Cite this

Yoshioka, H., Yoshiko, Y., Minamizaki, T., Suzuki, S., Koma, Y., Nobukiyo, A., ... Maeda, N. (2011). Incisor enamel formation is impaired in transgenic rats overexpressing the type III NaPi transporter Slc20a1. Calcified Tissue International, 89(3), 192-202. https://doi.org/10.1007/s00223-011-9506-0
Yoshioka, Hirotaka ; Yoshiko, Yuji ; Minamizaki, Tomoko ; Suzuki, Sayaka ; Koma, Yoshiro ; Nobukiyo, Asako ; Sotomaru, Yusuke ; Suzuki, Atsushi ; Itoh, Mitsuyasu ; Maeda, Norihiko. / Incisor enamel formation is impaired in transgenic rats overexpressing the type III NaPi transporter Slc20a1. In: Calcified Tissue International. 2011 ; Vol. 89, No. 3. pp. 192-202.
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Yoshioka, H, Yoshiko, Y, Minamizaki, T, Suzuki, S, Koma, Y, Nobukiyo, A, Sotomaru, Y, Suzuki, A, Itoh, M & Maeda, N 2011, 'Incisor enamel formation is impaired in transgenic rats overexpressing the type III NaPi transporter Slc20a1', Calcified Tissue International, vol. 89, no. 3, pp. 192-202. https://doi.org/10.1007/s00223-011-9506-0

Incisor enamel formation is impaired in transgenic rats overexpressing the type III NaPi transporter Slc20a1. / Yoshioka, Hirotaka; Yoshiko, Yuji; Minamizaki, Tomoko; Suzuki, Sayaka; Koma, Yoshiro; Nobukiyo, Asako; Sotomaru, Yusuke; Suzuki, Atsushi; Itoh, Mitsuyasu; Maeda, Norihiko.

In: Calcified Tissue International, Vol. 89, No. 3, 01.09.2011, p. 192-202.

Research output: Contribution to journalArticle

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T1 - Incisor enamel formation is impaired in transgenic rats overexpressing the type III NaPi transporter Slc20a1

AU - Yoshioka, Hirotaka

AU - Yoshiko, Yuji

AU - Minamizaki, Tomoko

AU - Suzuki, Sayaka

AU - Koma, Yoshiro

AU - Nobukiyo, Asako

AU - Sotomaru, Yusuke

AU - Suzuki, Atsushi

AU - Itoh, Mitsuyasu

AU - Maeda, Norihiko

PY - 2011/9/1

Y1 - 2011/9/1

N2 - Inorganic phosphate (Pi) is required in many biological processes, including signaling cascades, skeletal development, tooth mineralization, and nucleic acid synthesis. Recently, we showed that Pi transport in osteoblasts, mediated by Slc20a1, a member of the type III sodium-dependent phosphate transporter family, is indispensable for osteoid mineralization in rapidly growing rat bone. In addition, we found that bone mineral density decreased slightly with dysfunction of Pi homeostasis in aged transgenic rats overexpressing mouse Slc20a1 (Slc20a1-Tg). Bone and tooth share certain common molecular features, and thus, we focused on tooth development in Slc20a1-Tg mandibular incisors in order to determine the role of Slc20a1 in tooth mineralization. Around the time of weaning, there were no significant differences in serologic parameters between wild-type and Slc20a1-Tg rats. However, histological analysis showed that Slc20a1-Tg ameloblasts formed clusters in the papillary layer during the maturation stage as early as 4 weeks of age. These pathologies became more severe with age and included the formation of cyst-like or multilayer ameloblast structures, accompanied by a chalky white appearance with abnormal attrition and fracture. Hyperphosphatemia was also observed in aging Slc20a1-Tg rats. Micro-computed tomography and electron probe microanalysis revealed impairments in enamel, such as delayed mineralization and hypomineralization. Our results suggest that enamel formation is sensitive to imbalances in Pit1-mediated cellular function as seen in bone, although these processes are under the control of systemic Pi homeostasis.

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