Bone Abstracts

Fibroblast growth factor-23 (FGF23) is a hormone originating from osteocytes with suppressive actions on renal phosphate reabsorption and vitamin D synthesis. We recently identified FGF23 as a calcium-conserving hormone, regulating the membrane transport of the epithelial calcium channel TRPV5 in distal renal tubules. Here, we analyzed the long term sequelae of Fgf23 deficiency and renal calcium wasting on bone and mineral metabolism in 9-month-old mice lacking both Fgf23<...

Lack of Klotho, the co-receptor for the bone-derived hormone fibroblast growth factor-23 (FGF23), leads to a severe impairment in bone mineralization in mice. However, the mechanisms underlying the Klotho deficiency-associated defects in bone mineralization are still poorly understood. Here, we sought to elucidate the vitamin D independent role of Klotho in bone mineralization. To ablate increased vitamin D signaling in Klotho knockout mice (Kl−/−), we c...

It is well known that the epidermal growth factor receptor (EGFR), its ligands, and the structurally related receptor ERBB2/neu are expressed in skeletal cells. However, the functions of EGFR ligands in bone cells remain poorly defined. In this study, we employed a transgenic mouse line overexpressing the EGFR ligand amphiregulin (AREG) specifically in osteoblasts under the α1(I)-collagen promoter. AREG-tg mice did not show changes in body weight or gross phenotype. Compa...

Background: The tyrosine kinase inhibitor (TKI) imatinib is applied as front-line treatment in adult and pediatric patients with chronic myeloid leukemia (CML) in order to selectively inhibit the causative oncogenic BCR-ABL1 tyrosine kinase. However, TKIs exhibit off-target effects on further kinases involved in the regulation of bone metabolism. As consequence, pediatric patients display longitudinal growth retardation while on imatinib treatment. As CML is a rare disease in ...