| First Author | Gardiner EM | Year | 2000 |
| Journal | FASEB J | Volume | 14 |
| Issue | 13 | Pages | 1908-16 |
| PubMed ID | 11023975 | Mgi Jnum | J:64973 |
| Mgi Id | MGI:1891535 | Doi | 10.1096/fj.99-1075com |
| Citation | Gardiner EM, et al. (2000) Increased formation and decreased resorption of bone in mice with elevated vitamin D receptor in mature cells of the osteoblastic lineage. FASEB J 14(13):1908-16 |
| abstractText | The microarchitecture of bone is regulated by complex interactions between the bone-forming and resorbing cells, and several compounds regulate both actions. For example, vitamin D, which is required for bone mineralization, also stimulates bone resorption. Transgenic mice overexpressing the vitamin D receptor solely in mature cells of the osteoblastic bone-forming lineage were generated to test the potential therapeutic value of shifting the balance of vitamin D activity in favor of bone formation. Cortical bone was 5% wider and 15% stronger in these mice due to a doubling of periosteal mineral apposition rate without altered body weight or calcium homeostatic hormone levels. A 20% increase in trabecular bone volume in transgenic vertebrae was also observed, unexpectedly associated with a 30% reduction in resorption surface rather than greater bone formation. These findings indicate anabolic vitamin D activity in bone and identify a previously unknown pathway from mature osteoblastic cells to inhibit osteoclastic bone resorption, counterbalancing the known stimulatory action through immature osteoblastic cells. A therapeutic approach that both stimulates cortical anabolic and inhibits trabecular resorptive pathways would be ideal for treatment of osteoporosis and other osteopenic disorders.-Gardiner, E. M., Baldock, P. A., Thomas, G. P., Sims, N. A., Henderson, N. K., Hollis, B., White, C. P., Sunn, K. L., Morrison, N. A., Walsh, W. R., Eisman, J. A. Increased formation and decreased resorption of bone in mice with elevated vitamin D receptor in mature cells of the osteoblastic lineage. |
