title: Comparative study of mesenchymal stem cells from C57BL/10 and mdx mice.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Neurology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, ProC. liyong999@yahoo.com
authors.forename: Yong
authors.initials: Y
authors.lastname: Li
authors.forename: Cheng
authors.initials: C
authors.lastname: Zhang
authors.forename: Fu
authors.initials: F
authors.lastname: Xiong
authors.forename: Mei-juan
authors.initials: MJ
authors.lastname: Yu
authors.forename: Fu-Lin
authors.initials: FL
authors.lastname: Peng
authors.forename: Yan-chang
authors.initials: YC
authors.lastname: Shang
authors.forename: Cui-ping
authors.initials: CP
authors.lastname: Zhao
authors.forename: Yong-feng
authors.initials: YF
authors.lastname: Xu
authors.forename: Zheng-shan
authors.initials: ZS
authors.lastname: Liu
authors.forename: Chang
authors.initials: C
authors.lastname: Zhou
authors.forename: Jin-lang
authors.initials: JL
authors.lastname: Wu
mesh_terms: D000818:Animals; D018952:Antigens, CD34 / Q000096:biosynthesis* / Q000378:metabolism; D049109:Cell Proliferation; D002469:Cell Separation; D002478:Cells, Cultured; D003114:Colony-Forming Units Assay; D004195:Disease Models, Animal; D016189:Dystrophin / Q000172:deficiency / Q000235:genetics*; D005434:Flow Cytometry; D006801:Humans; D059630:Mesenchymal Stem Cells / Q000166:cytology / Q000473:pathology / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018101:Mice, Inbred mdx; D024510:Muscle Development / Q000235:genetics; D020388:Muscular Dystrophy, Duchenne / Q000235:genetics; D009154:Mutation / Q000235:genetics; D013045:Species Specificity
chemical_list: D018952:Antigens, CD34; D016189:Dystrophin