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Calcium and ER stress mediate hepatic apoptosis after burn injury
Article first published online: 26 NOV 2009
DOI: 10.1111/j.1582-4934.2008.00644.x
© 2009 The Authors Journal compilation © 2009 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd
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Jeschke, M. G., Gauglitz, G. G., Song, J., Kulp, G. A., Finnerty, C. C., Cox, R. A., Barral, J. M., Herndon, D. N. and Boehning, D. (2009), Calcium and ER stress mediate hepatic apoptosis after burn injury. Journal of Cellular and Molecular Medicine, 13: 1857–1865. doi: 10.1111/j.1582-4934.2008.00644.x
Publication History
- Issue published online: 26 NOV 2009
- Article first published online: 26 NOV 2009
- Received: July 22, 2008; Accepted: December 17, 2008
- Abstract
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References
- 1
- 2World Health Organization (WHO). A graphical overview of the global burden of injuries. The injury chart book. Volume 29. Geneva : WHO ; 2002.
- 3, . Support of the metabolic response to burn injury. Lancet. 2004; 363: 1895–902.
- 4, , , et al . Reversal of catabolism by beta-blockade after severe burns. N Engl J Med. 2001; 345: 1223–9.
- 5, , , et al . Intensive insulin therapy in critically ill patients. New Engl J Med. 2001; 345: 1359–67.
- 6, , , et al . Cytokine expression profile over time in severely burned pediatric patients. Shock. 2006; 26: 13–9.
- 7, , , et al . Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia. Nature. 1987; 330: 662–4.
- 8, , , et al . Cachectin/tumor necrosis factor induces lethal shock and stress hormone responses in the dog. Surg Gynecol Obstet. 1987; 164: 415–22.
- 9. Cytokines and the hepatic acute phase response. J Pathol. 1997; 181: 257–66.
- 10, , , et al . Cell proliferation, apoptosis, NF-kappaB expression, enzyme, protein, and weight changes in livers of burned rats. Am J Physiol Gastrointest Liver Physiol. 2001; 280: G1314–20.
- 11, , , et al . Changes in liver function and size after a severe thermal injury. Shock. 2007; 28: 172–7.
- 12, , , et al . Insulin prevents liver damage and preserves liver function in lipopolysaccharide-induced endotoxemic rats. J Hepatol. 2005; 42: 870–9.
- 13, , , et al . Insulin treatment improves hepatic morphology and function through modulation of hepatic signals after severe trauma. Ann Surg. 2004; 240: 340–9.
- 14, , , et al . Liver disease in burn injury: evidence from a national sample of 31,338 adult patients. J Burns Wounds. 2007; 7: e1.
- 15, , . Extended hypermetabolic response of the liver in severely burned pediatric patients. Arch Surg. 2004; 139: 641–7.
- 16, . Cell death in health and disease. J Cell Mol Med. 2007; 11: 1214–24.
- 17. Apoptosis-based therapies. Nat Rev Drug Discov. 2002; 1: 111–21.
- 18, . Death receptor activation-induced hepatocyte apoptosis and liver injury. Curr Mol Med. 2003; 3: 491–508.
- 19, , . Development and analysis of a small animal model simulating the human postburn hypermetabolic response. J Surg Res. 1978; 25: 394–403.
- 20, . Functional properties of recombinant type I and type III inositol 1, 4,5-trisphosphate receptor isoforms expressed in COS-7 cells. J Biol Chem. 2000; 275: 21492–9.
- 21, , , et al . Cytochrome c binds to inositol (1,4,5) trisphosphate receptors, amplifying calcium-dependent apoptosis. Nat Cell Biol. 2003; 5: 1051–61.
- 22, , , et al . Requirement of biphasic calcium release from the endoplasmic reticulum for Fas-mediated apoptosis. J Cell Biol. 2006; 175: 709–14.
- 23, , , et al . Thapsigargin, a tumor promoter, discharges intracellular Ca2+ stores by specific inhibition of the endoplasmic reticulum Ca2(+)-ATPase. Proc Natl Acad Sci USA. 1990; 87: 2466–70.
- 24, , , et al . Ca2+ oscillations induced by hormonal stimulation of individual fura-2-loaded hepatocytes. J Biol Chem. 1989; 264: 12859–66.
- 25, , . Intraluminal calcium as a primary regulator of endoplasmic reticulum function. Cell Calcium. 2005; 38: 303–10.
- 26, , . The endoplasmic reticulum: folding, calcium homeostasis, signaling, and redox control. Antioxid Redox Signal. 2006; 8: 1391–418.
- 27, . Signal integration in the endoplasmic reticulum unfolded protein response. Nat Rev Mol Cell Biol. 2007; 8: 519–29.
- 28, , , et al . Lymphocyte apoptosis: mediation by increased type 3 inositol 1,4,5-trisphosphate receptor. Science. 1996; 273: 503–7.
- 29, , , et al . ER stress triggers apoptosis by activating BH3-only protein Bim. Cell. 2007; 129: 1337–49.
- 30, , , et al . Calcium in cell injury and death. Annu Rev Pathol. 2006; 1: 405–34.
- 31, , , et al . Type 3 inositol 1,4,5-trisphosphate receptor modulates cell death. FASEB J. 2000; 14: 1375–9.
- 32, , , et al . Bcl-X(L) affects Ca(2+) homeostasis by altering expression of inositol 1,4,5-trisphosphate receptors. Proc Natl Acad Sci USA. 2002; 99: 9830–5.
- 33, . T cells deficient in inositol 1,4,5-trisphosphate receptor are resistant to apoptosis. Mol Cell Biol. 1997; 17: 3005–12.
- 34, , , et al . Control of apoptosis by IP(3) and ryanodine receptor driven calcium signals. Cell Calcium. 2000; 28: 349–63.
- 35, , . Apoptosis driven by IP(3)-linked mitochondrial calcium signals. EMBO J. 1999; 18: 6349–61.
- 36, . IP3 receptors in cell survival and apoptosis: Ca2+ release and beyond. Apoptosis. 2007; 12: 951–68.
- 37, . Mechanisms of liver injury: an overview. Curr Mol Med. 2003; 3: 483–90.
- 38, , . The central role of Fas-ligand cell signaling in inflammatory lung diseases. J Cell Mol Med. 2004; 8: 285–93.
- 39, , , et al . Chemical chaperones reduce ER stress and restore glucose homeostasis in a mouse model of type 2 diabetes. Science. 2006; 313: 1137–40.
- 40, . A new pharmacology–drugging stressed folding pathways. Trends Mol Med. 2005; 11: 347–50.

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