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Regulation of osteoblast and osteoclast functions by FGF‐6

Regulation of osteoblast and osteoclast functions by FGF‐6 Fibroblast growth factor‐6 (FGF‐6) is known to be the key ligand for fibroblast growth factor receptor 4 (FGFR4) during muscle regeneration but its role in bone has yet to be verified. FGFR signaling is known to be important in the initiation and regulation of osteogenesis, so in this study the actions of FGF‐6 on human osteoblasts and osteoclasts were investigated. Human primary osteoblasts (hOB) were used to study the effect of FGF‐6 on proliferation (by ATP quantification), signal transduction (by ERK and AKT phosphorylation), differentiation (by alkaline phosphatase activity, APA), and mineralization (by calcein staining). To study FGF‐6 activity on osteoclast differentiation, human bone marrow cells were used and tartrate‐resistant acid phosphatase (TRAP) multinucleated cells together with actin filaments arrangements were quantified. Human primary mature osteoclasts were used to evaluate the effect of FGF‐6 on osteoclast reabsorbing activity by reabsorbed pit measurements. FGF‐6 >10−9 M as FGF‐2 10−7 M induced hOB proliferation mediated by pERK together with a reduction in APA and reduced mineralization of the treated cells. Moreover FGF‐6 increased the formation of TRAP‐positive multinucleated cells in a dose‐dependent manner (maximal effect at 10−8 M). FGF‐6‐treated cells showed also a greater percentage of cells that formed typical osteoclast sealing zones. Mature osteoclasts cultured on dentine slice increased the area of reabsorption with a maximal effect of FGF‐6 at 10−12 M. FGF‐6 may be considered a regulator of bone metabolism as shown by its activity on both osteoblasts and osteoclasts. J. Cell. Physiol. 225: 466–471, 2010. © 2010 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Cellular Physiology Wiley

Regulation of osteoblast and osteoclast functions by FGF‐6

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References (29)

Publisher
Wiley
Copyright
Copyright © 2010 Wiley‐Liss, Inc.
ISSN
0021-9541
eISSN
1097-4652
DOI
10.1002/jcp.22225
pmid
20458746
Publisher site
See Article on Publisher Site

Abstract

Fibroblast growth factor‐6 (FGF‐6) is known to be the key ligand for fibroblast growth factor receptor 4 (FGFR4) during muscle regeneration but its role in bone has yet to be verified. FGFR signaling is known to be important in the initiation and regulation of osteogenesis, so in this study the actions of FGF‐6 on human osteoblasts and osteoclasts were investigated. Human primary osteoblasts (hOB) were used to study the effect of FGF‐6 on proliferation (by ATP quantification), signal transduction (by ERK and AKT phosphorylation), differentiation (by alkaline phosphatase activity, APA), and mineralization (by calcein staining). To study FGF‐6 activity on osteoclast differentiation, human bone marrow cells were used and tartrate‐resistant acid phosphatase (TRAP) multinucleated cells together with actin filaments arrangements were quantified. Human primary mature osteoclasts were used to evaluate the effect of FGF‐6 on osteoclast reabsorbing activity by reabsorbed pit measurements. FGF‐6 >10−9 M as FGF‐2 10−7 M induced hOB proliferation mediated by pERK together with a reduction in APA and reduced mineralization of the treated cells. Moreover FGF‐6 increased the formation of TRAP‐positive multinucleated cells in a dose‐dependent manner (maximal effect at 10−8 M). FGF‐6‐treated cells showed also a greater percentage of cells that formed typical osteoclast sealing zones. Mature osteoclasts cultured on dentine slice increased the area of reabsorption with a maximal effect of FGF‐6 at 10−12 M. FGF‐6 may be considered a regulator of bone metabolism as shown by its activity on both osteoblasts and osteoclasts. J. Cell. Physiol. 225: 466–471, 2010. © 2010 Wiley‐Liss, Inc.

Journal

Journal of Cellular Physiology – Wiley

Published: Nov 1, 2010

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