期刊
BONE
卷 37, 期 1, 页码 25-31出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.bone.2005.02.021
关键词
osteopetrosis; TGF-beta; LTBP; osteoblasts; osteoclasts
资金
- NCI NIH HHS [CA 34282] Funding Source: Medline
- NIAMS NIH HHS [P01 AR 42919] Funding Source: Medline
- NIDCR NIH HHS [DE13742] Funding Source: Medline
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. (C) 2005 Elsevier Inc. All rights reserved.
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