title: CD90-positive cells, an additional cell population, produce laminin alpha2 upon transplantation to dy(3k)/dy(3k) mice.
abstract: Laminin alpha2 is a component of skeletal and cardiac muscle basal lamina. A defect of the laminin alpha2 chain leads to severe congenital muscular dystrophy (MDC1A) in humans and dy/dy mice. Myogenic cells including myoblasts, myotubes, and myofibers in skeletal muscle are a possible source of the laminin alpha2 chain, and myogenic cells are thus proposed as a cell source for congenital muscular dystrophy therapy. However, we observed production of laminin alpha2 in non-myogenic cells of normal mice, and we could enrich these laminin alpha2-producing cells in CD90(+) cell fractions. Intriguingly, the number of CD90(+) cells increased dramatically during skeletal muscle regeneration in mice. This fraction did not include myogenic cells but exhibited a fibroblast-like phenotype. Moreover, these cells were resident in skeletal muscle, not derived from bone marrow. Finally, the production of laminin alpha2 in CD90(+) cells was not dependent on fusion with myogenic cells. Thus, CD90(+) cells are a newly identified additional cell fraction that increased during skeletal muscle regeneration in vivo and could be another cell source for therapy for lama2-deficient muscular dystrophy.
authors.affiliation: Department of Immunology, Graduate School of Pharmaceutical Sciences, Osaka University, 1-6 Yamada-oka, Suita, Osaka 565-0871, Japan. fukada@phs.osaka-u.ac.jp
authors.forename: So-Ichiro
authors.initials: S
authors.lastname: Fukada
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: Masashi
authors.initials: M
authors.lastname: Segawa
authors.forename: Kenta
authors.initials: K
authors.lastname: Sakamoto
authors.forename: Mari
authors.initials: M
authors.lastname: Nakajima
authors.forename: Masaki
authors.initials: M
authors.lastname: Sato
authors.forename: Daisuke
authors.initials: D
authors.lastname: Morikawa
authors.forename: Akiyoshi
authors.initials: A
authors.lastname: Uezumi
authors.forename: Yuko
authors.initials: Y
authors.lastname: Miyagoe-Suzuki
authors.forename: Shin'ichi
authors.initials: S
authors.lastname: Takeda
authors.forename: Kazutake
authors.initials: K
authors.lastname: Tsujikawa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yamamoto
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D002469:Cell Separation / Q000379:methods; D048430:Cell Shape / Q000502:physiology; D002478:Cells, Cultured; D005260:Female; D005347:Fibroblasts / Q000378:metabolism* / Q000637:transplantation*; D007797:Laminin / Q000172:deficiency / Q000378:metabolism*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D024510:Muscle Development / Q000502:physiology; D018482:Muscle, Skeletal / Q000166:cytology / Q000378:metabolism*; D009136:Muscular Dystrophies / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D010641:Phenotype; D012038:Regeneration / Q000502:physiology; D033581:Stem Cell Transplantation / Q000379:methods; D013234:Stem Cells / Q000378:metabolism; D018800:Thy-1 Antigens / Q000378:metabolism*; D016378:Tissue Transplantation / Q000379:methods*
chemical_list: D015415:Biomarkers; D007797:Laminin; D018800:Thy-1 Antigens; C102645:laminin alpha 2