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Open Access Highly Accessed Research article

Comparative study of mesenchymal stem cells from C57BL/10 and mdx mice

Yong Li2, Cheng Zhang12*, Fu Xiong2, Mei-juan Yu2, Fu-lin Peng1, Yan-chang Shang1, Cui-ping Zhao1, Yong-feng Xu4, Zheng-shan Liu2, Chang Zhou1 and Jin-lang Wu3

Author Affiliations

1 Department of Neurology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, ProC

2 Stem Cells and Tissue Engineering Research Center, Sun Yat-Sen University, Guangzhou, Guangdong, ProC

3 Department of electron microscope, Sun Yat-Sen University, Guangzhou, Guangdong, ProC

4 Department of Neurology, Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, ProC

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BMC Cell Biology 2008, 9:24  doi:10.1186/1471-2121-9-24

Published: 19 May 2008



Human mesenchymal stem cells (MSCs) have been studied and applied extensively because of their ability to self-renew and differentiate into various cell types. Since most human diseases models are murine, mouse MSCs should have been studied in detail. The mdx mouse – a Duchenne muscular dystrophy model – was produced by introducing a point mutation in the dystrophin gene. To understand the role of dystrophin in MSCs, we compared MSCs from mdx and C57BL/10 mice, focusing particularly on the aspects of light and electron microscopic morphology, immunophenotyping, and differentiation potential.


Our study showed that at passage 10, mdx-MSCs exhibited increased heterochromatin, larger vacuoles, and more lysosomes under electron microscopy compared to C57BL/10-MSCs. C57BL/10-MSCs formed a few myotubes, while mdx-MSCs did not at the same passages. By passage 21, mdx-MSCs but not C57BL/10-MSCs had gradually lost their proliferative ability. In addition, a significant difference in the expression of CD34, not Sca-1 and CD11b, was observed between the MSCs from the 2 mice.


Our current study reveals that the MSCs from the 2 mice, namely, C57BL/10 and mdx, exhibit differences in proliferative and myogenic abilities. The results suggest that the changes in mouse MSC behavior may be influenced by lack of dystrophin protein in mdx mouse.