Burn Trauma Acutely Increases the Respiratory Capacity and Function of Liver Mitochondria. Issue 4 (April 2018)
- Record Type:
- Journal Article
- Title:
- Burn Trauma Acutely Increases the Respiratory Capacity and Function of Liver Mitochondria. Issue 4 (April 2018)
- Main Title:
- Burn Trauma Acutely Increases the Respiratory Capacity and Function of Liver Mitochondria
- Authors:
- Bohanon, Fredrick J.
Nunez Lopez, Omar
Herndon, David N.
Wang, Xiaofu
Bhattarai, Nisha
Ayadi, Amina E.
Prasai, Anesh
Jay, Jayson W.
Rojas-Khalil, Yesenia
Toliver-Kinsky, Tracy E.
Finnerty, Celeste C.
Radhakrishnan, Ravi S.
Porter, Craig - Abstract:
- ABSTRACT: Background: A complete understanding of the role of the liver in burn-induced hypermetabolism is lacking. We 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. Methods: Male BALB/c mice (8–12 weeks) received full-thickness scald burns on ∼30% of the body surface. Liver tissue was harvested 24 h postinjury. 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 ∼60% of the body surface. Serum was collected 24 h postinjury. HepG2 cells were cultured with serum-enriched media from either sham- or burn-treated rats. Protein levels were analyzed via western blot. Results: Mass-specific ( P = 0.01) and mitochondrial-specific ( P = 0.01) respiration coupled to ATP production significantly increased in the liver after burn. The respiratory control ratio for ADP ( P = 0.04) and the mitochondrial flux control ratio ( P = 0.03) were elevated in the liver of burned animals. Complex III and Complex IV protein abundance in the liver increased after burn by 17% and 14%, respectively. Exposure of HepG2 cells to serum from burned rats increased the pAMPKα:AMPKα ratio ( P < 0.001) and levels of SIRT1 ( P = 0.01), Nrf2 ( P < 0.001), and PGC1α ( P = 0.02). Conclusions: Severe burn traumaABSTRACT: Background: A complete understanding of the role of the liver in burn-induced hypermetabolism is lacking. We 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. Methods: Male BALB/c mice (8–12 weeks) received full-thickness scald burns on ∼30% of the body surface. Liver tissue was harvested 24 h postinjury. 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 ∼60% of the body surface. Serum was collected 24 h postinjury. HepG2 cells were cultured with serum-enriched media from either sham- or burn-treated rats. Protein levels were analyzed via western blot. Results: Mass-specific ( P = 0.01) and mitochondrial-specific ( P = 0.01) respiration coupled to ATP production significantly increased in the liver after burn. The respiratory control ratio for ADP ( P = 0.04) and the mitochondrial flux control ratio ( P = 0.03) were elevated in the liver of burned animals. Complex III and Complex IV protein abundance in the liver increased after burn by 17% and 14%, respectively. Exposure of HepG2 cells to serum from burned rats increased the pAMPKα:AMPKα ratio ( P < 0.001) and levels of SIRT1 ( P = 0.01), Nrf2 ( P < 0.001), and PGC1α ( P = 0.02). Conclusions: 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. … (more)
- Is Part Of:
- Shock. Volume 49:Issue 4(2018)
- Journal:
- Shock
- Issue:
- Volume 49:Issue 4(2018)
- Issue Display:
- Volume 49, Issue 4 (2018)
- Year:
- 2018
- Volume:
- 49
- Issue:
- 4
- Issue Sort Value:
- 2018-0049-0004-0000
- Page Start:
- Page End:
- Publication Date:
- 2018-04
- Subjects:
- Burns -- hypermetabolism -- liver -- mitochondria
Shock -- Periodicals
Shock -- Periodicals
Choc (Pathologie) -- Périodiques
Shock
Periodicals
616.0475 - Journal URLs:
- http://www.shockjournal.com ↗
http://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=toc&D=yrovft&AN=00024382-000000000-00000 ↗
http://journals.lww.com ↗ - DOI:
- 10.1097/SHK.0000000000000935 ↗
- Languages:
- English
- ISSNs:
- 1073-2322
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 8267.443000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 9093.xml