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Impaired bone anabolic response to parathyroid hormone in Fgf2-/- and Fgf2+/- mice
1University of Connecticut Health Center, Farmington, CT, USA. Hurley@nso1.uchc.edu
Abstract:
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 (80mug/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 (160mug/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.
Insights
Fibroblast growth factor 2 (FGF2) is crucial for the bone-building effects of parathyroid hormone (PTH). Mice lacking FGF2 showed significantly reduced responses to PTH treatment, indicating FGF2
Area of Science:
- Bone biology
- Endocrinology
- Skeletal research
Background:
- Parathyroid hormone (PTH) is known to stimulate bone formation.
- PTH increases fibroblast growth factor 2 (FGF2) expression in osteoblasts.
- Elevated serum FGF2 levels are observed in osteoporotic patients treated with PTH.
Purpose of the Study:
- To investigate whether the anabolic effect of PTH on bone is dependent on FGF2.
- To assess the role of endogenous FGF2 in mediating PTH-induced bone growth.
Main Methods:
- Treatment of wild-type (Fgf2+/+) and knockout (Fgf2-/-) mice with recombinant human PTH (rhPTH 1-34).
- Analysis of bone formation using micro-computed tomography (Micro-CT) and histomorphometry.
- Assessment of bone mineral density (BMD) via Dual-energy X-ray absorptiometry (DEXA).
Main Results:
- PTH significantly increased bone formation in Fgf2+/+ mice, but this effect was diminished in Fgf2-/- mice.
- Insulin-like growth factor 1 (IGF-1) levels were reduced in PTH-treated Fgf2-/- mice.
- DEXA analysis showed significant BMD increase in Fgf2+/+ mice, a minimal increase in Fgf2+/- mice, and a decrease in Fgf2-/- mice following PTH treatment.
Conclusions:
- Endogenous FGF2 is essential for achieving the maximal bone anabolic response to PTH in mice.
- FGF2 plays a critical role in mediating the skeletal effects of PTH.
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