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

Authors :
Xu Yong-feng
Zhao Cui-ping
Shang Yan-chang
Peng Fu-lin
Yu Mei-juan
Xiong Fu
Zhang Cheng
Li Yong
Liu Zheng-shan
Zhou Chang
Wu Jin-lang
Source :
BMC Cell Biology, Vol 9, Iss 1, p 24 (2008)
Publication Year :
2008
Publisher :
BMC, 2008.

Abstract

Abstract Background 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. Results 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. Conclusion 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.

Subjects

Subjects :
Cytology
QH573-671

Details

Language :
English
ISSN :
14712121
Volume :
9
Issue :
1
Database :
Directory of Open Access Journals
Journal :
BMC Cell Biology
Publication Type :
Academic Journal
Accession number :
edsdoj.f3ecafce8a8e430db2803f35c3786e7c
Document Type :
article
Full Text :
https://doi.org/10.1186/1471-2121-9-24