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低剂量 X 射线辐射可刺激小鼠颅骨成骨细胞的分化和矿化。

X-ray radiation at low doses stimulates differentiation and mineralization of mouse calvarial osteoblasts.

机构信息

Department of Orthodontics, Chonbuk National University, Jeonju, Korea.

出版信息

BMB Rep. 2012 Oct;45(10):571-6. doi: 10.5483/bmbrep.2012.45.10.101.

DOI:10.5483/bmbrep.2012.45.10.101
PMID:23101511
Abstract

Radiotherapy is considered to cause detrimental effects on bone tissue eventually increasing bone loss and fracture risk. However, there is a great controversy on the real effects of irradiation itself on osteoblasts, and the mechanisms by which irradiation affects osteoblast differentiation and mineralization are not completely understood. We explored how X-ray radiation influences differentiation and bone-specific gene expression in mouse calvarial osteoblasts. Irradiation at 2 Gy not only increased differentiation and mineralization of the cells, but also upregulated the expression of alkaline phosphatase, type I collagen, osteopontin, and osteocalcin at early stages of differentiation. However, irradiation at higher doses (>2 Gy) did not stimulate osteoblast differentiation, rather it suppressed DNA synthesis by the cells without a toxic effect. Additional experiments suggested that transforming growth factor-beta 1 and runt-transcription factor 2 play important roles in irradiation- stimulated bone differentiation by acting as upstream regulators of bone-specific markers.

摘要

放射治疗被认为最终会对骨组织造成有害影响,增加骨质流失和骨折风险。然而,关于照射本身对成骨细胞的实际影响存在很大争议,并且照射影响成骨细胞分化和矿化的机制尚未完全阐明。我们探讨了 X 射线辐射如何影响小鼠颅骨成骨细胞的分化和骨特异性基因表达。2 Gy 的照射不仅增加了细胞的分化和矿化,还在分化的早期上调了碱性磷酸酶、I 型胶原、骨桥蛋白和骨钙素的表达。然而,更高剂量(>2 Gy)的照射并没有刺激成骨细胞分化,而是在没有毒性作用的情况下抑制了细胞的 DNA 合成。额外的实验表明,转化生长因子-β1 和 runt 转录因子 2 通过作为骨特异性标志物的上游调节剂,在照射刺激骨分化中发挥重要作用。

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