A comparative study of bone marrow mesenchymal stem cell functionality in C57BL and mdx mice
A comparative study of bone marrow mesenchymal stem cell functionality in C57BL and mdx mice
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C57BL和mdx小鼠骨髓间充质干细胞功能的比较研究
DOI：
10.1016/j.neulet.2012.06.061
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发表时间：
2012-08-15
影响因子：
2.5
通讯作者：
Zhang, Weixi
中科院分区：
文献类型：
--
作者：
Leng, Yan;Zheng, Zhenyang;Zhang, Weixi
DMD患者骨量低，骨折发生率高，但这种病理情况背后的细胞和分子机制尚不清楚。由于骨髓间充质干细胞(BMSCs)是成骨细胞的前体细胞，我们推测DMD导致BMSCs分化功能障碍。我们从C57BL对照小鼠和MDX突变小鼠(已建立的DMD小鼠模型)中分离出BMSCs，并比较它们的增殖、分化能力和谱系特异性基因的表达。结果表明，mdx鼠骨髓间充质干细胞的增殖、成骨分化和肌源性分化均明显低于C57BL鼠。由于dystrophin基因突变导致DMD，我们的结果表明dystrophin缺乏导致BMSCs的分化和增殖功能障碍。(C)2012爱思唯尔爱尔兰有限公司。保留所有权利。
Patients with DMD have low bone mass and a high incidence of fractures, but the cellular and molecular mechanisms underlying this pathological condition are unknown. Because bone marrow mesenchymal stem cells (BMSCs) are the progenitors of bone-forming osteoblasts, we hypothesized that DMD leads to dysfunction in the differentiation of BMSCs. We isolated BMSCs from C57BL control and mdx mutant mice, a well-established mouse model of DMD, and compared their abilities of proliferation, differentiation, and the expression of lineage-specific genes. Results showed that the proliferation and osteogenic and myogenic differentiation of BMSCs from mdx mice were significantly lower than those from C57BL mice. Because mutations in dystrophin gene cause DMD, our results demonstrate that dystrophin deficiency leads to dysfunction in the differentiation and proliferation of BMSCs. (C) 2012 Elsevier Ireland Ltd. All rights reserved.