Impaired bone anabolic response to parathyroid hormone in Fgf2-/- and Fgf2+/- mice

M. M. Hurley, Y. Okada, L. Xiao, Y. Tanaka, M. Ito, N. Okimoto, T. Nakamura, C. J. Rosen, T. Doetschman, J. D. Coffin

Research output: Contribution to journalArticlepeer-review

78 Scopus citations


Since parathyroid hormone (PTH) increased FGF2 mRNA and protein expression in osteoblasts, and serum FGF-2 was increased in osteoporotic patients treated with PTH, we assessed whether the anabolic effect of PTH was impaired in Fgf2-/- mice. Eight-week-old Fgf2+/+ and Fgf2-/- male mice were treated with rhPTH 1-34 (80 μg/kg) for 4 weeks. Micro-CT and histomorphometry demonstrated that PTH significantly increased parameters of bone formation in femurs from Fgf2+/+ mice but the changes were smaller and not significant in Fgf2-/- mice. IGF-1 was significantly reduced in serum from PTH-treated Fgf2-/- mice. DEXA analysis of femurs from Fgf2+/+, Fgf2+/-, and Fgf2-/- mice treated with rhPTH (160 μg/kg) for 10 days showed that PTH significantly increased femoral BMD in Fgf2+/+ by 18%; by only 3% in Fgf2+/- mice and reduced by 3% in Fgf2-/- mice. We conclude that endogenous Fgf2 is important for maximum bone anabolic effect of PTH in mice.

Original languageEnglish (US)
Pages (from-to)989-994
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number4
StatePublished - Mar 24 2006
Externally publishedYes


  • Bone formation
  • DEXA
  • Fgf2 haploinsufficient
  • Fgf2 null
  • Mice
  • Micro-CT
  • PTH

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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