Nature Genetics
- 38, 1424 - 1429 (2006)
Published online: 12 November 2006; | doi:10.1038/ng1916
BMP2 activity, although dispensable for bone formation, is required for the initiation of fracture healingKunikazu Tsuji1, Amitabha Bandyopadhyay2, Brian D Harfe3, Karen Cox1, Sanjeev Kakar4, Louis Gerstenfeld4, Thomas Einhorn4, Clifford J Tabin2 & Vicki Rosen11
Department of Developmental Biology, Harvard School of Dental Medicine, Boston, Massachusetts 02115, USA. 2
Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA. 3
Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, Florida 32610, USA. 4
Department of Orthopedics, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Correspondence should be addressed to Vicki Rosen vicki_rosen@hsdm.harvard.edu Adult bones have a notable regenerative capacity. Over 40 years ago, an intrinsic activity capable of initiating this reparative response was found to reside within bone itself, and the term bone morphogenetic protein1 (BMP) was coined to describe the molecules responsible for it. A family of BMP proteins was subsequently identified2,
3,
4, but no individual BMP has been shown to be the initiator of the endogenous bone repair response. Here we demonstrate that BMP2 is a necessary component of the signaling cascade that governs fracture repair. Mice lacking the ability to produce BMP2 in their limb bones have spontaneous fractures that do not resolve with time. In fact, in bones lacking BMP2, the earliest steps of fracture healing seem to be blocked. Although other osteogenic stimuli are still present in the limb skeleton of BMP2-deficient mice, they cannot compensate for the absence of BMP2. Collectively, our results identify BMP2 as an endogenous mediator necessary for fracture repair.
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