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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
PubMed

Insights

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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