Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/125989
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Type: Journal article
Title: Fibroblast growth factor receptor 3 deficiency does not impair the osteoanabolic action of parathyroid hormone on mice
Author: Xie, Y.
Yi, L.
Weng, T.
Huang, J.
Luo, F.
Jiang, W.
Xian, C.
Du, X.
Chen, L.
Citation: International Journal of Biological Sciences, 2017; 12(8):990-999
Publisher: Ivyspring International Publisher
Issue Date: 2017
ISSN: 1449-2288
1449-2288
Statement of
Responsibility: 
Yangli Xie, Lingxian Yi, Tujun Weng, Junlan Huang, Fengtao Luo ... Cory J Xian ... et al.
Abstract: Summary: PTH stimulates bone formation in Fgfr3 knockout mice through promotion of proliferation and differentiation in osteoblasts. Introduction: Previous studies showed that endogenous fibroblast growth factor 2 (FGF-2) is required for parathyroid hormone (PTH)-stimulated bone anabolic effects, however, the exact mechanisms by which PTH stimulate bone formation and the function of FGF receptors in mediating these actions are not fully defined. FGF receptor 3 (FGFR3) has been characterized as an important regulator of bone metabolism and is confirmed to cross-talk with PTH/PTHrP signal in cartilage and bone development. Methods: Fgfr3 knockout and wild-type mice at 2-month-old and 4-month-old were intraperitoneally injected with PTH intermittently for 4 weeks and then the skeletal responses to PTH were assessed by dual energy X-ray absorptiometry (DEXA), micro-computed tomography (μCT) and bone histomorphometry. Results: Intermittent PTH treatment improved bone mineral density (BMD) and femoral mechanical properties in both Fgfr3-/- and wild-type mice. Histomorphometric analysis showed that bone formation and bone resorption were increased in both genotypes following PTH treatment. PTH treatment increased trabecular bone volume (BV/TV) in WT and Fgfr3-deficient mice. The anabolic response in Fgfr3-deficient and wild-type bone is characterized by an increase of both bone formation and resorption-related genes following PTH treatment. In addition, we found that Fgfr3 null osteoblasts (compared to wild-type controls) maintained normal abilities to response to PTH-stimulated increase of proliferation, differentiation, expression of osteoblastic marker genes (Cbfa1, Osteopontin and Osteocalcin), and phosphorylation of Erk1/2. Conclusions: Bone anabolic effects of PTH were not impaired by the absence of FGFR3, suggesting that the FGFR3 signaling may not be required for osteoanabolic effects of PTH activities.
Keywords: PTH; FGFR3; knockout mice; bone remodeling; osteoblast
Rights: This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) License. See http://ivyspring.com/terms for full terms and conditions.
DOI: 10.7150/ijbs.14077
Appears in Collections:Aurora harvest 8
Biochemistry publications

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