A comparative study of bone marrow mesenchymal stem cell functionality in C57BL and mdx mice

Yan Leng, Zhenyang Zheng, Chen Zhou, Cheng Zhang, Xing Ming Shi, Weixi Zhang

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)139-144
Number of pages6
JournalNeuroscience Letters
Volume523
Issue number2
DOIs
StatePublished - Aug 15 2012

Keywords

  • Bone marrow mesenchymal stem cells
  • Mdx mice
  • Osteogenic differentiation
  • Proliferation

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'A comparative study of bone marrow mesenchymal stem cell functionality in C57BL and mdx mice'. Together they form a unique fingerprint.

  • Cite this