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Calciprotein particles regulate fibroblast growth factor-23 expression in osteoblasts.

Ken-Ichi Akiyama1, Yutaka Miura2, Hirosaka Hayashi2

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PubMed
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Calciprotein particles, formed from calcium and phosphate, signal osteoblasts to release fibroblast growth factor-23 (FGF23). This hormone helps maintain phosphate balance by increasing kidney excretion.

Keywords:
amorphous calcium-phosphatecrystalline calcium-phosphatefetuin-Aosteoblasts

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Area of Science:

  • Biochemistry
  • Mineral Metabolism
  • Cell Biology

Background:

  • Fibroblast growth factor-23 (FGF23) is crucial for phosphate homeostasis, secreted by osteoblasts/osteocytes to regulate kidney phosphate excretion.
  • The precise mechanism by which bone cells sense dietary phosphate remains largely unknown.

Purpose of the Study:

  • To investigate the role of calciprotein particles in sensing phosphate and regulating FGF23 production.
  • To elucidate the relationship between calciprotein particle characteristics and FGF23 induction.

Main Methods:

  • In vitro studies using cultured osteoblastic cells with varying calcium and phosphate concentrations.
  • In vivo studies in mice involving phosphate administration and intravenous injection of calciprotein particles.
  • In vivo imaging to track calciprotein particle distribution.

Main Results:

  • Increased calcium or phosphate in vitro induced FGF23 expression, dependent on calciprotein particle formation.
  • Blocking the amorphous-to-crystalline transition of precipitates enhanced FGF23 expression, suggesting amorphous particles are potent inducers.
  • Phosphate loading in mice increased circulating calciprotein particles and FGF23 levels.
  • In vivo imaging confirmed calciprotein particles reach osteoblasts within bone marrow.

Conclusions:

  • Calciprotein particles act as phosphate sensors in bone cells.
  • Osteoblasts likely induce FGF23 secretion in response to elevated extracellular calciprotein particles after phosphate ingestion.
  • This mechanism provides a novel insight into phosphate metabolism regulation.