Burn trauma acutely increases the respiratory capacity and function of liver mitochondria

Model System:

Burn

Reference Type:

Journal article

Accession No.:

J81110

Journal:

Shock

Year, Volume, Issue, Page(s):

2018 , 49, 4, 466-473

Publication Website:

Abstract:

Study investigated the acute effect of severe burn trauma on liver mitochondrial respiratory capacity and coupling control as well as the signaling events underlying these alterations. Male BALB/c mice (8–12 weeks) received full-thickness scald burns on approximately 30 percent of the body surface. Liver tissue was harvested 24 hours post injury. Mitochondrial respiration was determined by high-resolution respirometry. Citrate synthase activity was determined as a proxy of mitochondrial density. Male Sprague-Dawley rats received full-thickness scald burns to approximately60 percent of the body surface. Serum was collected 24 hours post injury. HepG2 cells were cultured with serum-enriched media from either sham- or burn-treated rats. Protein levels were analyzed via western blot. Mass-specific and mitochondrial-specific respiration coupled to ATP production significantly increased in the liver after burn. The respiratory control ratio for ADP and the mitochondrial flux control ratio were elevated in the liver of burned animals. Complex III and Complex IV protein abundance in the liver increased after burn by 17 percent and 14 percent, respectively. Exposure of HepG2 cells to serum from burned rats increased the ratio of phosphorylated to total AMPKα and levels of SIRT1, Nrf2, and PGC1α. Findings indicate that severe burn trauma augments respiratory capacity and function of liver mitochondria, adaptations that augment ATP production. This response may be mediated by systemic factors that activate signaling proteins responsible for regulating cellular energy metabolism and mitochondrial biogenesis.

Author(s):