| First Author | Dabovic B | Year | 2005 |
| Journal | Bone | Volume | 37 |
| Issue | 1 | Pages | 25-31 |
| PubMed ID | 15878314 | Mgi Jnum | J:123830 |
| Mgi Id | MGI:3719740 | Doi | 10.1016/j.bone.2005.02.021 |
| Citation | Dabovic B, et al. (2005) Osteopetrosis-like phenotype in latent TGF-beta binding protein 3 deficient mice. Bone 37(1):25-31 |
| abstractText | LTBPs are extracellular matrix proteins resembling fibrillins. LTBP-1, 3, and 4 covalently bind latent TGF-beta and modulate tissue levels of this potent cytokine through regulation of its secretion, localization, and/or activation. To address LTBP function in vivo, we generated Ltbp-3 null mice. Ltbp-3-/- animals developed craniofacial abnormalities due to early ossification of the skull base synchondroses and displayed reduced body size. In addition, histological examination of Ltbp-3-/- skeletons revealed an increase in bone mass. The osteoblast numbers and mineral apposition rates were decreased in Ltbp-3-/- mice, whereas the osteoclast numbers were similar in null and wild type mice. Histological examination revealed persistence of cartilage remnants in Ltbp-3-/- trabecular bone. Taken together, these results indicate that the Ltbp-3-/- high bone mass phenotype was due to a defect in bone resorption. We hypothesize that lack of Ltbp-3 results in decreased levels of TGF-beta in bone and cartilage, which leads to compromised osteoclast function and decreased bone turnover. |
