title: Temporal study following burn injury in young rats is associated with skeletal muscle atrophy, inflammation and altered myogenic regulatory factors.
abstract: BACKGROUND
  Burn injury (BI) greater than 40% has been associated with protein catabolism and it is characterized by a hypermetabolic response followed for muscle loss.
  
  
  OBJECTIVE
  The purpose of this study was to investigate the temporal effects of extensive experimental BI in the skeletal muscle distant from lesion, through morphological analysis, expression of genes related to muscle atrophy, inflammation and the myogenic regulatory factors.
  
  
  METHODS
  A total of 60 young male wistar rats were distributed into two groups, control (C) and subjected to scald burn injury (SBI). The animals were euthanized 1, 4 and 14 days post-sham or 45% of the total body surface BI. The medial head of gastrocnemii muscles were submitted to histopathological, morphometric (muscle fibers area and density), MyoD and myogenin immunoexpression, and gene expression for TNF-α, iNOS and E3 ubiquitin ligases (MuRF1 and MAFbx).
  
  
  RESULTS
  Histopathological findings were consistent with increased amount of connective tissue and inflammatory process. Muscle fiber area of SBI groups was smaller than C and no differences were found in fiber muscle density. TNF-α was higher in SBI groups, one and 14 days post-injury; iNOS expression was higher on the first and fourth day post-injury. MuRF-1 was higher on the day four and MAFbx on the day 14.
  
  
  CONCLUSIONS
  In conclusion, BI causes inflammation, atrophy and myogenesis stimulation in muscle as a result of systemic host response.
authors.affiliation: Department of Biosciences, Federal University of Sao Paulo, UNIFESP, Rua Silva Jardim, 136-Lab 328, Santos, SP, 11015-020, Brazil.
authors.forename: Hananiah Tardivo
authors.initials: HT
authors.lastname: Quintana
authors.forename: Jeferson André
authors.initials: JA
authors.lastname: Bortolin
authors.forename: Nathalia Trasmonte
authors.initials: NT
authors.lastname: da Silva
authors.forename: Flavia Andressa Pidone
authors.initials: FA
authors.lastname: Ribeiro
authors.forename: Edson Aparecido
authors.initials: EA
authors.lastname: Liberti
authors.forename: Daniel Araki
authors.initials: DA
authors.lastname: Ribeiro
authors.forename: Flavia
authors.initials: F
authors.lastname: de Oliveira
mesh_terms: D000818:Animals; D002056:Burns / Q000150:complications*; D007249:Inflammation / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D023421:Models, Animal; D018485:Muscle Fibers, Skeletal / Q000473:pathology; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology*; D009133:Muscular Atrophy / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D017570:MyoD Protein / Q000378:metabolism; D018006:Myogenic Regulatory Factors / Q000378:metabolism*; D018008:Myogenin / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D044767:Ubiquitin-Protein Ligases / Q000378:metabolism
chemical_list: D017570:MyoD Protein; D018006:Myogenic Regulatory Factors; D018008:Myogenin; D014409:Tumor Necrosis Factor-alpha; D052247:Nitric Oxide Synthase Type II; D044767:Ubiquitin-Protein Ligases