title: The expression patterns of Pax7 in satellite cells during overload-induced rat adult skeletal muscle hypertrophy.
abstract: OBJECTIVE
  Activated satellite cells (SCs) have the ability to reacquire a quiescent, undifferentiated state. Pax7 plays a crucial role in allowing activated SCs to undergo self-renewal. Because the increase in the SC population is induced during overload-induced skeletal muscle hypertrophy, it is possible that Pax7-regulated SC self-renewal is involved in the modulation of the SC population during the functional overload of skeletal muscles. However, the characteristics of the expression patterns of Pax7 in SCs during the functional overload of adult skeletal muscles are poorly understood.
  
  
  METHODS
  Using immunohistochemical approaches, we examined the temporal and spatial expression patterns of Pax7 expressed in SCs during the functional overloading of rat skeletal muscles.
  
  
  RESULTS
  The time course of Pax7 expression in SCs was similar to that of the expression of the differentiation regulatory factor myogenin during the early stage of functional overload. However, the percentage of SCs that expressed Pax7 was markedly higher than that of the SCs that expressed myogenin. Coexpression of Pax7 and myogenin was not detected in SCs. In addition, the expression of cyclin-dependent kinase inhibitor p21, which regulates cell cycle arrest and differentiation, was not detected in Pax7-positive SCs.
  
  
  CONCLUSIONS
  These results suggest that Pax7-regulated self-renewal of SCs may be induced during the early stage of functional overload and may contribute to modulating the SC population in hypertrophied muscles. Furthermore, it was suggested that the numbers of SCs which underwent self-renewal may be higher than that of SCs which were provided as the additional myonuclei for hypertrophying myofibres.
authors.affiliation: Osaka University of Health and Sport Sciences, Japan. m-ishido@auecc.aichi-edu.ac.jp
authors.forename: M
authors.initials: M
authors.lastname: Ishido
authors.forename: M
authors.initials: M
authors.lastname: Uda
authors.forename: N
authors.initials: N
authors.lastname: Kasuga
authors.forename: M
authors.initials: M
authors.lastname: Masuhara
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D049109:Cell Proliferation; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism; D005260:Female; D006984:Hypertrophy; D007150:Immunohistochemistry; D018482:Muscle, Skeletal / Q000473:pathology*; D009135:Muscular Diseases / Q000209:etiology / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D018008:Myogenin / Q000378:metabolism; D051761:Paired Box Transcription Factors / Q000378:metabolism*; D005082:Physical Exertion; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D051381:Rats; D011916:Rats, Inbred F344; D032496:Satellite Cells, Skeletal Muscle / Q000378:metabolism* / Q000473:pathology; D013997:Time Factors; D014018:Tissue Distribution
chemical_list: D050759:Cyclin-Dependent Kinase Inhibitor p21; D018008:Myogenin; C530821:PAX7 protein, rat; D051761:Paired Box Transcription Factors; D018809:Proliferating Cell Nuclear Antigen