Research ArticlePhysiology

DDR2 (discoidin domain receptor 2) suppresses osteoclastogenesis and is a potential therapeutic target in osteoporosis

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Science Signaling  24 Mar 2015:
Vol. 8, Issue 369, pp. ra31
DOI: 10.1126/scisignal.2005835

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Reorganizing receptor complexes to rebuild bone

The skeleton undergoes continuous turnover mediated by osteoblasts and osteoclasts, which respectively deposit and resorb bone. When this turnover is dysregulated, skeletal diseases such as osteoporosis—a disease characterized by bone loss—can occur. The receptor tyrosine kinase DDR2 (discoidin domain receptor 2) tilts the balance in favor of bone formation. Zhang et al. determined that, in addition to promoting osteoblast differentiation, DDR2 inhibited osteoclast differentiation and bone matrix resorption in culture. In a mouse model of osteoporosis, viral-mediated delivery of DDR2 increased bone density. By forming a complex with the receptors Neuropilin-1 and PlexinA1, DDR2 blocked PlexinA1-mediated stimulation of osteoclastogenesis. Thus, increasing the abundance of DDR2 in both types of bone precursor cells may be therapeutically beneficial for osteoporosis patients.

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