Increased bone formation in osteocalcin-deficient mice
Increased bone formation in osteocalcin-deficient mice
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DOI：
10.1038/382448a0
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发表时间：
1996-08-01
期刊：
影响因子：
64.8
通讯作者：
Karsenty, G
中科院分区：
文献类型：
--
作者：
Ducy, P;Desbois, C;Karsenty, G
脊椎动物不断重塑骨骼。破骨细胞对原有骨的吸收和成骨细胞对新骨的形成是严格协调的，以将骨量维持在限定的限度内。影响破骨细胞活性的骨重建的分子决定因素（1-3）已被表征，但成骨细胞活性的分子决定因素尚不清楚。为了研究骨钙素（最丰富的成骨细胞特异性非胶原蛋白（4））的作用，我们产生了骨钙素缺陷小鼠。这些小鼠发展出以更高的骨量和改善的功能质量的骨为标志的表型。卵巢切除术前后的组织形态学研究表明，骨钙素的缺乏导致骨形成增加，而不损害骨吸收。据我们所知，这项研究提供了第一个证据，骨钙素是骨形成的决定因素。
VERTEBRATES constantly remodel bone. The resorption of preexisting bone by osteoclasts and the formation of new hone by osteoblasts is strictly coordinated to maintain bone mass within defined limits. A fen molecular determinants of bone remodelling that affect osteoclast activity(1-3) have been characterized, bot the molecular determinants of osteoblast activity are unknown. To investigate the role of osteocalcin, the most abundant osteoblast-specific non-collagenous protein(4) we have generated osteocalcin-deficient mice. These mice develop a phenotype marked by higher bone mass and bones of Improved functional quality. Histomorphometric studies done before and after ovariectomy showed that the absence of osteocalcin leads to an increase in bone formation without impairing bone resorption. To our knowledge, this study provides the first evidence that osteocalcin is a determinant of bone formation.