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Published on: August 26, 2013
PDGF inhibits BMP2-induced bone healing
Sanja Novak1, Josip Madunic1,2, Laura Shum1
1Center for Regenerative Medicine and Skeletal Development, UConn Health, Farmington, CT, USA.
Abstract:
Bone regeneration depends on a pool of bone/cartilage stem/progenitor cells and signaling mechanisms regulating their differentiation. Using in vitro approach, we have shown that PDGF signaling through PDGFRβ inhibits BMP2-induced osteogenesis, and significantly attenuates expression of BMP2 target genes. We evaluated outcomes of treatment with two anabolic agents, PDGF and BMP2 using different bone healing models. Targeted deletion of PDGFRβ in αSMA osteoprogenitors, led to increased callus bone mass, resulting in improved biomechanical properties of fractures. In critical size bone defects BMP2 treatment increased proportion of osteoprogenitors, while the combined treatment of PDGF BB with BMP2 decreased progenitor number at the injury site. BMP2 treatment induced significant bone formation and increased number of osteoblasts, while in contrast combined treatment with PDGF BB decreased osteoblast numbers. This is in vivo study showing that PDGF inhibits BMP2-induced osteogenesis, but inhibiting PDGF signaling early in healing process does not improve BMP2-induced bone healing.
Insights
Platelet-derived growth factor (PDGF) inhibits bone formation induced by bone morphogenetic protein 2 (BMP2). Inhibiting PDGF signaling early in healing did not improve BMP2-driven bone healing in vivo.
Area of Science:
- Regenerative Medicine
- Skeletal Biology
- Cell Signaling
Background:
- Bone regeneration relies on stem/progenitor cells and signaling pathways.
- Platelet-derived growth factor (PDGF) signaling via PDGF receptor beta (PDGFRβ) is known to inhibit bone morphogenetic protein 2 (BMP2)-induced osteogenesis in vitro.
Purpose of the Study:
- To evaluate the in vivo effects of PDGF and BMP2 on bone healing.
- To determine if inhibiting PDGF signaling improves BMP2-mediated bone regeneration.
Main Methods:
- Utilized in vivo bone healing models.
- Investigated outcomes of PDGF BB and BMP2 treatments.
- Examined targeted deletion of PDGFRβ in alpha-smooth muscle actin (αSMA) osteoprogenitors.
Main Results:
- Targeted deletion of PDGFRβ in osteoprogenitors increased callus bone mass and improved fracture biomechanics.
- BMP2 treatment increased osteoprogenitors, while combined PDGF BB and BMP2 treatment decreased progenitor numbers.
- BMP2 treatment enhanced osteoblast numbers; combined PDGF BB and BMP2 treatment reduced osteoblast numbers.
Conclusions:
- In vivo, PDGF inhibits BMP2-induced osteogenesis.
- Early inhibition of PDGF signaling does not enhance BMP2-induced bone healing.
- PDGF signaling negatively impacts BMP2-driven bone formation and osteoprogenitor availability.
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