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Endogenous FGF-2 is critically important in PTH anabolic effects on bone
Maria Giovanna Sabbieti1, Dimitrios Agas, Liping Xiao
1Department of Comparative Morphology and Biochemistry, University of Camerino, Camerino (MC), Italy.
Journal of Cellular Physiology
|December 25, 2008
Summary
Fibroblast growth factor-2 (FGF-2) is crucial for parathyroid hormone (PTH) to stimulate osteoblast proliferation, differentiation, and survival. Reduced FGF-2 impairs the anabolic response to PTH.
Area of Science:
- Bone biology
- Endocrinology
- Cell signaling
Background:
- Parathyroid hormone (PTH) is a key anabolic regulator of bone.
- Fibroblast growth factor-2 (FGF-2) is implicated in PTH's anabolic effects.
- FGF-2 deficiency reduces the anabolic response to PTH.
Purpose of the Study:
- To investigate how FGF-2 deficiency affects PTH-mediated signaling in osteoblasts.
- To identify candidate factors modulated by FGF-2 in PTH's anabolic response.
Main Methods:
- Comparison of osteoblasts from wild-type (Fgf2+/+) and FGF-2 knockout (Fgf2-/-) mice.
- Analysis of Runx-2, CREB phosphorylation, cell cycle proteins (cyclinD1-cdk4/6, p21/waf1), and apoptosis markers (Bcl-2/Bax ratio).
- Immunocytochemistry and Western blot techniques were employed.
Main Results:
- PTH increased Runx-2 and CREB phosphorylation in Fgf2+/+ osteoblasts, but not in Fgf2-/- osteoblasts.
- FGF-2 silencing in Fgf2+/+ osteoblasts blocked PTH's effects on Runx-2 and CREB.
- PTH promoted osteoblast proliferation and survival in Fgf2+/+ cells, while increasing cell cycle inhibition in Fgf2-/- cells.
Conclusions:
- Endogenous FGF-2 is essential for PTH-induced osteoblast proliferation, differentiation, and apoptosis regulation.
- Reduced FGF-2 expression contributes to the blunted anabolic response to PTH observed in Fgf2-/- mice.
- The anabolic effects of PTH are, in part, dependent on FGF-2 expression.
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