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首页> 外文期刊>Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research >Zinc-finger transcription factor odd-skipped related 2 is one of the regulators in osteoblast proliferation and bone formation.
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Zinc-finger transcription factor odd-skipped related 2 is one of the regulators in osteoblast proliferation and bone formation.

机译：锌指转录因子与奇异相关2是成骨细胞增殖和骨形成的调节因子之一。

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We report that Osr2 is one of the regulators of osteoblast function, because dominant-negative Osr2 transgenic mice exhibited decreased osteoblast activity and delayed mineralization in calvarial and tibial bone tissues. Our results indicate that Osr2 functions in regulation of osteoblast proliferation. INTRODUCTION: Molecular mechanisms that control bone formation have received attention with increasing knowledge related to genetic control of osteoblast differentiation. The odd-skipped related (Osr) gene is a zinc-finger transcription factor recently suggested to be involved in bone formation, although little is known about its role. MATERIALS AND METHODS: To elucidate the in vivo function of Osr2, we generated transgenic mice overexpressing dominant-negative Osr2. RESULTS: In this study, N-terminal-deleted Osr2 was found to act as a dominant-negative mutant toward both Osr1 and Osr2. Dominant-negative Osr2 (Osr2DeltaN) transgenic mice showed delayed mineralization in calvarial and cortical bone tissues. Furthermore, soft X-ray analysis of transgenic mice bones revealed distinctly increased radiolucency. Examinations of newborn Osr2DeltaN transgenic mice skeletons stained with alcian blue and alizarin red showed reduced intensities in the skull and skeletal elements. Morphologically, calvariae and tibias of Osr2DeltaN transgenic mice were composed of markedly thinner parietal and cortical bones and lower numbers of osteoblastic cells on bone surfaces, indicating a reduced proliferation of osteoblasts. Furthermore, calvarial osteoblasts obtained from Osr2DeltaN transgenic mice showed highly attenuated osteoblast differentiation and proliferation, confirming that Osr2 is needed for osteogenesis. Finally, results of Runx2-deficient cell assays suggested that Osr2 induces alkaline phosphatase (ALP) expression, but to a lesser degree than Runx2-expressing cells. CONCLUSIONS: Our genetic observations showed that the Osr2 gene plays a key role in osteoblastic cell proliferation.
机译：我们报告Osr2是成骨细胞功能的调节剂之一，因为显性阴性的Osr2转基因小鼠表现出成骨细胞活性降低和颅盖和胫骨骨组织矿化延迟。我们的结果表明，Osr2在调节成骨细胞增殖中起作用。引言：随着成骨细胞分化的遗传控制相关知识的不断发展，控制骨骼形成的分子机制已受到关注。跳过相关的基因（Osr）是一种锌指转录因子，最近被认为与骨骼形成有关，尽管对其作用知之甚少。材料与方法：为了阐明Osr2的体内功能，我们产生了过表达显性负性Osr2的转基因小鼠。结果：在这项研究中，发现N-末端缺失的Osr2对Osr1和Osr2均起显性负突变作用。显性负性Osr2（Osr2DeltaN）转基因小鼠在颅盖和皮质骨组织中显示出矿化延迟。此外，对转基因小鼠骨骼进行的软X射线分析表明，其放射线透明度明显增加。阿尔辛蓝和茜素红染色的新生Osr2DeltaN转基因小鼠骨骼检查显示头骨和骨骼元素强度降低。从形态上讲，Osr2DeltaN转基因小鼠的颅盖和胫骨由明显较薄的顶骨和皮质骨以及较少的骨表面成骨细胞组成，表明成骨细胞的增殖减少。此外，从Osr2DeltaN转基因小鼠获得的颅盖成骨细胞显示出高度减毒的成骨细胞分化和增殖，证实Osr2是成骨作用所必需的。最后，Runx2缺陷细胞分析的结果表明，Osr2诱导碱性磷酸酶（ALP）表达，但程度低于表达Runx2的细胞。结论：我们的遗传观察表明，Osr2基因在成骨细胞增殖中起关键作用。

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