title: A comparative study of bone marrow mesenchymal stem cell functionality in C57BL and mdx mice.
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.
authors: Department of Neurology, The First Affiliated Hospital, Sun Yat-sen University, No. 58 Zhongshan Road 2, Guangzhou 510080, China.
authors: Yan
authors: Y
authors: Leng
authors: Zhenyang
authors: Z
authors: Zheng
authors: Chen
authors: C
authors: Zhou
authors: Cheng
authors: C
authors: Zhang
authors: XingMing
authors: X
authors: Shi
authors: Weixi
authors: W
authors: Zhang
mesh_terms: D000818:Animals; D001854:Bone Marrow Cells / Q000166:cytology / Q000502:physiology*; D002454:Cell Differentiation; D019070:Cell Lineage; D049109:Cell Proliferation; D002478:Cells, Cultured; D020869:Gene Expression Profiling; D008297:Male; D059630:Mesenchymal Stem Cells / Q000166:cytology / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018101:Mice, Inbred mdx; D018482:Muscle, Skeletal / Q000473:pathology; D020388:Muscular Dystrophy, Duchenne / Q000235:genetics / Q000473:pathology; D013045:Species Specificity