Caveolin‐1 Knockout Mice Have Increased Bone Size and Stiffness

Caveolin‐1 Knockout Mice Have Increased Bone Size and Stiffness
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DOI:
10.1359/jbmr.070601
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发表时间:
2007-09
影响因子:
6.2
通讯作者:
J. Rubin;Z. Schwartz;B. Boyan;X. Fan;N. Case;Buer Sen;Marcus Drab;Deborah Smith;M. Aleman;K. L. Wong;Hai Yao;H. Jo;T. Gross
J. Rubin;Z. Schwartz;B. Boyan;X. Fan;N. Case;Buer Sen;Marcus Drab;Deborah Smith;M. Aleman;K. L. Wong;Hai Yao;H. Jo;T. Gross
中科院分区:
医学1区
文献类型:
--
作者:
J. Rubin;Z. Schwartz;B. Boyan;X. Fan;N. Case;Buer Sen;Marcus Drab;Deborah Smith;M. Aleman;K. L. Wong;Hai Yao;H. Jo;T. Gross

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对缺陷窝的CAV-1−/−小鼠的骨骼表型进行了检测。μ、CT和组织学检查显示,该基因缺失导致骨小梁和皮质骨增多。伴随着结构变化的是力学性能的提高。细胞研究表明,Cav-1缺乏会导致成骨细胞分化增加。这些结果表明,Cav-1有助于维持成骨细胞前体细胞处于较低分化状态。
The skeletal phenotype of the cav‐1−/− mouse, which lacks caveolae, was examined. μCT and histology showed increased trabecular and cortical bone caused by the gene deletion. Structural changes were accompanied by increased mechanical properties. Cell studies showed that cav‐1 deficiency leads to increased osteoblast differentiation. These results suggest that cav‐1 helps to maintain osteoblast progenitors in a less differentiated state.