Ryoko Yamamoto

Hiroshima University, Hiroshima-shi, Hiroshima-ken, Japan

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Publications (6)15.63 Total impact

  • Orthodontic Waves 03/2012; 71(1):40. DOI:10.1016/j.odw.2011.12.004
  • Orthodontic Waves 03/2011; 70(1):47-47. DOI:10.1016/j.odw.2010.11.013
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    ABSTRACT: Osteoblasts/osteocytes are the principle sources of fibroblast growth factor 23 (FGF23), a phosphaturic hormone, but the regulation of FGF23 expression during osteoblast development remains uncertain. Because 1alpha,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) and inorganic phosphate (Pi) may act as potent activators of FGF23 expression, we estimated how these molecules regulate FGF23 expression during rat osteoblast development in vitro. 1,25(OH)(2)D(3)-dependent FGF23 production was restricted largely to mature cells in correlation with increased vitamin D receptor (VDR) mRNA levels, in particular, when Pi was present. Pi alone and more so in combination with 1,25(OH)(2)D(3) increased FGF23 production and VDR mRNA expression. Parathyroid hormone, stanniocalcin 1, prostaglandin E(2), FGF2, and foscarnet did not increase FGF23 mRNA expression. Thus, these results suggest that 1,25(OH)(2)D(3) may exert its largest effect on FGF23 expression/production when exposed to high levels of extracellular Pi in osteoblasts/osteocytes.
    Journal of Endocrinology 09/2010; 206(3):279-86. DOI:10.1677/JOE-10-0058 · 3.72 Impact Factor
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    ABSTRACT: This report describes the treatment of a case of severe open bite with posterior crossbite. While treating open bite, the outcome may not always be successful with orthodontic therapy alone. In such cases, surgical therapy is often chosen to gain a stable occlusion. Skeletal anchorage systems such as miniscrews are now frequently used for correcting severe malocclusion. In this report, we treated an open bite by intruding the molars with miniscrews placed bilaterally in the interdental space between both the upper and lower posterior teeth. The active treatment period was 36 months and the patient's teeth continued to be stable after a retention period of 36 months.
    Australian Dental Journal 12/2009; 54(4):374-80. DOI:10.1111/j.1834-7819.2009.01166.x · 1.10 Impact Factor
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    ABSTRACT: Fibroblast growth factor (FGF)23 is produced primarily in bone and acts on kidney as a systemic phosphaturic factor; high levels result in rickets and osteomalacia. However, it remains unclear whether FGF23 acts locally and directly on bone formation. We overexpressed human FGF23 in a stage-specific manner during osteoblast development in fetal rat calvaria (RC) cell cultures by using the adenoviral overexpression system and analyzed its effects on osteoprogenitor proliferation, osteoid nodule formation, and mineralization. Bone formation was also measured by calcein labeling in parietal bone organ cultures. Finally, we addressed the role of tyrosine phosphorylation of FGF receptor (FGFR) in mineralized nodule formation. Nodule formation and mineralization, but not osteoprogenitor proliferation, were independently suppressed by overexpression of FGF23 in RC cells. Increased FGF23 levels also suppressed bone formation in the parietal bone organ culture model. FGF23 overexpression enhanced phosphorylation of FGFR, whereas the impairment of mineralized nodule formation by FGF23 overexpression was abrogated by SU5402, an inhibitor of FGFR1 tyrosine kinase activity. These studies suggest that FGF23 overexpression suppresses not only osteoblast differentiation but also matrix mineralization independently of its systemic effects on Pi homeostasis.
    Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 07/2008; 23(6):939-48. DOI:10.1359/jbmr.080220 · 6.83 Impact Factor
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    ABSTRACT: While fibroblast growth factor (FGF) 23 is known as a phosphaturic factor in inherited and/or acquired hypophosphatemic disorders, it also serves an endocrine role in normal phosphate homeostasis. FGF23 acts negatively on the NaPi2a cotransporter and 25-hydroxy D(3)-1 alpha-hydroxylase with a resultant decrease in renal phosphate (Pi) reabsorption, while osteoblasts appear to be a primary source of FGF23 whose expression is counter-upregulated by 1 alpha,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)). Here we have shown the distribution of FGF23 in normal rat bone and tooth, and its expression profile in fetal rat calvaria (RC) cell cultures. FGF23 mRNA was detectable in multiple fetal and adult tissues but levels were much higher in adult calvaria, femur and incisor, compared to the other tissues tested. Immunoreactive FGF23 was predominantly localized to osteoblasts, cementoblasts, and odontoblasts, with sporadic labeling in some chondrocytes, osteocytes and cementocytes. Notably, osteoclasts were also found to be a possible source of FGF23. Fetal bone and tooth germ cells labeled much less intensely than young adult osteoblasts and odontoblasts. In the RC cell model, FGF23 was expressed during osteoblast development. During matrix mineralization induced by beta-glycerophosphate (beta GP), FGF23 expression was transiently upregulated and then decreased to levels lower than in their non-beta GP-treated counterparts. 1,25(OH)(2)D(3) markedly increased FGF23 expression concomitant with the inhibition of beta GP-induced mineralization. Our data suggest that FGF23 expression in bone is closely correlated with bone formation in vitro and vivo, and points towards an important role(s) for FGF23 in young adult but not fetal mineralized tissues as a systemic factor for Pi homeostasis.
    Bone 07/2007; 40(6):1565-73. DOI:10.1016/j.bone.2007.01.017 · 3.97 Impact Factor

Publication Stats

227 Citations
15.63 Total Impact Points


  • 2010–2011
    • Hiroshima University
      • Department of Orthodontics and Craniofacial Developmental Biology
      Hiroshima-shi, Hiroshima-ken, Japan