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Osteoblast-derived FGF9 regulates skeletal homeostasis
Liping Wang1, Theresa Roth2, Marcia Abbott2
1Endocrine Unit, VA Medical Center, San Francisco, CA, USA; Department of Medicine, University of California, San Francisco, CA, USA.
Bone
|February 13, 2017
Summary
Osteoblast-derived FGF9 is crucial for maintaining skeletal homeostasis in male mice. Deleting the Fgf9 gene in osteoblasts led to decreased bone mass and formation, highlighting FGF9's regulatory role.
Area of Science:
- Skeletal Biology
- Endocrinology
- Cell Signaling
Background:
- Fibroblast Growth Factor 9 (FGF9) plays a role in skeletal development.
- FGF9 expression in osteoblasts (OBs) is modulated by G protein signaling.
- The specific contribution of OB-derived FGF9 to skeletal homeostasis is not fully understood.
Purpose of the Study:
- To investigate the role of osteoblast-derived FGF9 in maintaining skeletal homeostasis.
- To determine the effects of deleting Fgf9 in osteoblasts on bone mass and formation.
- To elucidate the mechanism by which FGF9 influences osteogenic progenitor cells.
Main Methods:
- Generation of a conditional knockout mouse model (Fgf9OB-/-) by deleting Fgf9 in osteoblasts using a Cre-lox system.
- Phenotypic analysis of bone mass and microarchitecture in Fgf9OB-/- mice and littermate controls.
- In vitro studies on mouse bone marrow stromal cells (BMSCs) treated with exogenous FGF9 to assess effects on mineralization and proliferation.
Main Results:
- Male Fgf9OB-/- mice exhibited significantly reduced cancellous bone and bone formation in the distal femur, along with decreased cortical thickness.
- Female Fgf9OB-/- mice did not show significant alterations in bone mass.
- Acute FGF9 treatment of BMSCs increased progenitor proliferation via Akt1 activation, while continuous treatment inhibited mineralization.
Conclusions:
- Mature osteoblasts are a significant source of FGF9, which positively regulates skeletal homeostasis in male mice.
- Osteoblast-derived FGF9 may act in a paracrine manner to sustain the osteogenic progenitor cell pool.
- FGF9 signaling, through Akt activation, is important for maintaining bone health.
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