title: Prenatal myonuclei play a crucial role in skeletal muscle hypertrophy in rodents.
abstract: Multinucleated muscle fibers are formed by the fusion of myogenic progenitor cells during embryonic and fetal myogenesis. However, the role of prenatally incorporated myonuclei in the skeletal muscle fibers of adult animals is poorly understood. We demonstrated, using muscle-specific reporter mice, that the prenatal myonuclei remained in the adult soleus muscle, although cardiotoxin injection caused the loss of prenatal myonuclei. Overloading by the tendon transection of synergists failed to induce compensatory hypertrophy in regenerated soleus muscle fibers of adult rats, whereas unloading by tail suspension normally induced the fiber atrophy. Loss of hypertrophying function correlated with the lowered histone acetylation at the transcription start site ofIgf1rgene, which was one of the genes that did not respond to the overloading. These parameters were improved by the transplantation of cells harvested from the juvenile soleus muscles of neonatal rats in association with enhanced histone acetylation ofIgf1rgene. These results indicated that the presence of prenatal myonuclei was closely related to the status of histone acetylation, which could regulate the responsiveness of muscle fibers to physiological stimuli.
authors.affiliation: Graduate School of Health Sciences, Matsumoto University, Matsumoto, Japan; fuminori.kawano@matsu.ac.jp.
authors.forename: Fuminori
authors.initials: F
authors.lastname: Kawano
authors.affiliation: Graduate School of Biomedical Science, Nagasaki University, Nagasaki, Japan.
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Ono
authors.affiliation: Graduate School of Biomedical Science, Nagasaki University, Nagasaki, Japan.
authors.forename: Ryo
authors.initials: R
authors.lastname: Fujita
authors.affiliation: Graduate School of Health Sciences, Matsumoto University, Matsumoto, Japan.
authors.forename: Atsuya
authors.initials: A
authors.lastname: Watanabe
authors.affiliation: Graduate School of Health Sciences, Matsumoto University, Matsumoto, Japan.
authors.forename: Ryo
authors.initials: R
authors.lastname: Masuzawa
authors.affiliation: Graduate School of Health Sciences, Matsumoto University, Matsumoto, Japan.
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Shibata
authors.affiliation: School of Engineering Science, Osaka University, Toyonaka, Japan.
authors.forename: Shunsuke
authors.initials: S
authors.lastname: Hasegawa
authors.affiliation: Graduate School of Medicine, Osaka University, Suita, Japan; and.
authors.forename: Ken
authors.initials: K
authors.lastname: Nakata
authors.affiliation: School of Human Cultures, University of Shiga Prefecture, Hikone, Japan.
authors.forename: Naoya
authors.initials: N
authors.lastname: Nakai
mesh_terms: D000107:Acetylation; D000818:Animals; D002478:Cells, Cultured; D005260:Female; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D018485:Muscle Fibers, Skeletal / Q000378:metabolism* / Q000473:pathology*; D009136:Muscular Dystrophies / Q000378:metabolism* / Q000473:pathology*; D017208:Rats, Wistar; D017526:Receptor, IGF Type 1 / Q000378:metabolism*
chemical_list: D017526:Receptor, IGF Type 1
keywords: histone modification; injury; myonucleus; regeneration; skeletal muscle fiber