BACKGROUND/AIMS: Fibroblast growth factor 23 (FGF23) has been shown to suppress parathyroid hormone (PTH) secretion. alpha-Klotho has been demonstrated to function as a fibroblast growth factor receptor (FGFR) cofactor for FGF23. Thus, both alpha-Klotho and FGFR may play roles in PTH synthesis and/or secretion. Functions of alpha-Klotho and FGFR in secondary hyperparathyroidism (SHPT) remain to be studied. The present studies explore the role of alpha-Klotho and FGFR in SHPT. METHODS: Hyperplastic parathyroid glands (n = 44) were obtained from patients with SHPT. RESULTS: Immunohistochemical study showed that both alpha-Klotho and FGFR1c expression in hyperplastic glands was significantly decreased compared with that in normal glands (Klotho p < 0.01, and FGFR1c p < 0.05). A significant positive correlation was observed between alpha-Klotho and FGFR1c (r(2) = 0.375, p < 0.01) indicating a cooperative system. Both alpha-Klotho (r(2) = 0.235, p < 0.05) and FGFR1c (r(2) = 0.181, p < 0.05) correlated positively with the calcium-sensing receptor (CaR), which plays an important role in the development of SHPT. In addition, expression of alpha-Klotho correlated negatively with parathyroid cell proliferation, as confirmed by Ki67 staining (r(2) = 0.148, p < 0.05). CONCLUSION: Decreased expression of alpha-Klotho and FGFR1c in parallel with CaR expression and parathyroid cell growth may be involved in the pathogenesis of SHPT. 2010 S. Karger AG, Basel.
BACKGROUND/AIMS: Fibroblast growth factor 23 (FGF23) has been shown to suppress parathyroid hormone (PTH) secretion. alpha-Klotho has been demonstrated to function as a fibroblast growth factor receptor (FGFR) cofactor for FGF23. Thus, both alpha-Klotho and FGFR may play roles in PTH synthesis and/or secretion. Functions of alpha-Klotho and FGFR in secondary hyperparathyroidism (SHPT) remain to be studied. The present studies explore the role of alpha-Klotho and FGFR in SHPT. METHODS: Hyperplastic parathyroid glands (n = 44) were obtained from patients with SHPT. RESULTS: Immunohistochemical study showed that both alpha-Klotho and FGFR1c expression in hyperplastic glands was significantly decreased compared with that in normal glands (Klotho p < 0.01, and FGFR1c p < 0.05). A significant positive correlation was observed between alpha-Klotho and FGFR1c (r(2) = 0.375, p < 0.01) indicating a cooperative system. Both alpha-Klotho (r(2) = 0.235, p < 0.05) and FGFR1c (r(2) = 0.181, p < 0.05) correlated positively with the calcium-sensing receptor (CaR), which plays an important role in the development of SHPT. In addition, expression of alpha-Klotho correlated negatively with parathyroid cell proliferation, as confirmed by Ki67 staining (r(2) = 0.148, p < 0.05). CONCLUSION: Decreased expression of alpha-Klotho and FGFR1c in parallel with CaR expression and parathyroid cell growth may be involved in the pathogenesis of SHPT. 2010 S. Karger AG, Basel.
Authors: Joerg Latus; Renate Lehmann; Meike Roesel; Peter Fritz; Niko Braun; Christoph Ulmer; Wolfgang Steurer; Dagmar Biegger; German Ott; Juergen Dippon; M Dominik Alscher; Martin Kimmel Journal: Endocrine Date: 2013-01-20 Impact factor: 3.633
Authors: María E Rodriguez-Ortiz; Ignacio Lopez; Juan R Muñoz-Castañeda; Julio M Martinez-Moreno; Alan Peralta Ramírez; Carmen Pineda; Antonio Canalejo; Philippe Jaeger; Escolastico Aguilera-Tejero; Mariano Rodriguez; Arnold Felsenfeld; Yolanda Almaden Journal: J Am Soc Nephrol Date: 2012-05-10 Impact factor: 10.121