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Cells of extraembryonic mesodermal origin confer human dystrophin in the Mdx model of duchenne muscular dystrophy
Author(s) -
Kawamichi Yayoi,
Cui ChangHao,
Toyoda Masashi,
Makino Hatsune,
Horie Akane,
Takahashi Yoriko,
Matsumoto Kenji,
Saito Hirohisa,
Ohta Hiroaki,
Saito Kayoko,
Umezawa Akihiro
Publication year - 2010
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.22076
Subject(s) - myogenesis , biology , duchenne muscular dystrophy , dystrophin , mesoderm , microbiology and biotechnology , placenta , amniotic epithelial cells , muscular dystrophy , fetus , anatomy , embryonic stem cell , myocyte , adult stem cell , genetics , pregnancy , gene
Duchenne muscular dystrophy is an X‐linked recessive genetic disease characterized by severe skeletal muscular degeneration. The placenta is considered to be a promising candidate cell source for cellular therapeutics because it contains a large number of cells and heterogenous cell populations with myogenic potentials. We analyzed the myogenic potential of cells obtained from six parts of the placenta, that is, umbilical cord, amniotic epithelium, amniotic mesoderm, chorionic plate, villous chorion, and decidua basalis. In vitro cells derived from amniotic mesoderm, chorionic plate, and villous chorion efficiently transdifferentiate into myotubes. In addition, in vivo implantation of placenta‐derived cells into dystrophic muscles of immunodeficient mdx mice restored sarcolemmal expression of human dystrophin. Differential contribution to myogenesis in this study may be attributed to placental portion‐dependent default cell state. Molecular taxonomic characterization of placenta‐derived maternal and fetal cells in vitro will help determine the feasibility of cell‐based therapy. J. Cell. Physiol. 223:695–702, 2010. © 2010 Wiley‐Liss, Inc.