| Theme | Recent advances in research concerning FGF23 and Klotho | |
|---|---|---|
| Title | Biological function of osteocyte and FGF23 -- Comparison between klotho deficient mice and wild-type mice | |
| Publish Date | 2012/01 | |
| Author | Hiromi Hongo | Department of Developmental Biology of Hard Tissue, Graduate School of Dental Medicine, Hokkaido University |
| Author | Muneteru Sasaki | Department of Developmental Biology of Hard Tissue, Graduate School of Dental Medicine, Hokkaido University |
| Author | Tomoka Hasegawa | Department of Developmental Biology of Hard Tissue, Graduate School of Dental Medicine, Hokkaido University |
| Author | Norio Amizuka | Department of Developmental Biology of Hard Tissue, Graduate School of Dental Medicine, Hokkaido University |
| [ Summary ] | Osteocytes make up functional syncytia, i.e., the osteocytic lacunar-canalicular system, and synthesize FGF23, sclerostin and DMP-1 which regulate serum concentrations of phosphorus, osteoblastic activity and the local mineralization, respectively. Transmembrane klotho is a primary co-receptor in FGF23-derived signaling pathways. Klotho deficient mice exhibited enhanced synthesis of DMP-1 but reduced amounts of FGF23, as well as several dying osteocytes and osteocytic lacunae occupying mineralized matrices. In klotho deficient mice, the broad unmineralized areas in secondary trabecules were observed despite premature mineralization in the primary trabecules, which indicates that once deposited, bone minerals can not be maintained, due to disrupted osteocytic function in klotho deficient bone. | |