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作 者:刘洪[1] 丁风云[1] 颜成东[1] 管铨成[1] 郑阳玉[2]
机构地区:[1]盐城卫生职业技术学院,江苏盐城224005 [2]南京医科大学口腔医学研究所,江苏南京210029
出 处:《口腔生物医学》2011年第3期131-135,139,共6页Oral Biomedicine
基 金:盐城市医学科技发展计划项目资助(YK2010112)
摘 要:目的:探讨1,25二羟维生素D3(1,25(OH)2D3)在小鼠下颌骨矿化中的作用机制。方法:利用组织学、免疫组织化学和实时定量RT-PCR比较分析了6周龄野生型和1α羟化酶基因敲除(1α(OH)ase-/-)小鼠下颌骨矿化的差异。结果:与野生型小鼠相比,1α(OH)ase-/-小鼠的类骨质的比例明显增加,骨钙素(osteocalcin,OCN)在下颌骨沉积面积和在成骨细胞表达水平均明显降低,碱性磷酸酶(ALP)在下颌骨成骨细胞的活性和表达水平明显降低,而Biglycan在下颌骨的沉积面积和在成骨细胞表达水平则明显增加。结论:1,25(OH)2D3通过调节OCN、ALP和Biglycan的基因表达水平和蛋白质沉积水平促进小鼠下颌骨的矿化。Objective:To determine the role of 1,25 (OH) 2 D3 in mandible mineralization of mice. Methods:The differences of the mandible mineralization between the wild-type and 1-α-hydroxylase gene knockout mice at 6 weeks old were assessed by histology, immunohistochemistry and real-time RT-PCR. Results:The ratio of osteoid volume was increased significantly, the deposition of osteocalcin (OCN) in mandible and the expressions of osteocalcin in the osteoblasts were reduced significantly, the active and the expression of alkaline phosphatase (ALP) in osteoblasts were also reduced significantly in 1-α-hydroxylase gene knockout mice compared to that in the wild-type littermate. But the deposition of Biglycan in the mandible and the expression of Biglycan in the osteoblasts were increased in 1-α-hydroxylase gene knockout mice. Conclusions: These results suggest that 1,25 (OH) 2 D3 promote mineralization of mandible of mice by regulating OCN, ALP and Biglycan genes expression and protein deposition.
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