Vagal nerve stimulation protects cardiac injury by attenuating mitochondrial dysfunction in a murine burn injury model

Journal of Cellular and Molecular Medicine

Volumn 17, Issue 5, 2013, Pages 664-671

  Lu, Xiaojiong ^a   Costantini, Todd ^a   Lopez, Nicole E ^a   Wolf, Paul L ^a   Hageny, Ann Marie ^a   Putnam, James ^a   Eliceiri, Brian ^a   Coimbra, Raul ^a  

^a UNIVERSITY OF CALIFORNIA SAN DIEGO   (United States)

Author keywords

Burn injury; Cardiac injury; Mitochondrial dysfunction; Mitochondrial swelling; PI3K Akt; Vagal nerve stimulation

Indexed keywords

ADENOSINE TRIPHOSPHATE; APOPTOSIS INDUCING FACTOR; CYTOCHROME C; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN BAD; PROTEIN BCL 2; PROTEIN KINASE B;

ANIMAL; APOPTOSIS; ARTICLE; BAGG ALBINO MOUSE; BURN; CYTOSOL; DISEASE MODEL; ENZYMOLOGY; HEART MITOCHONDRION; HEART MUSCLE; HEART MUSCLE CELL; MALE; METABOLISM; MITOCHONDRION SWELLING; MOUSE; PATHOLOGY; PHOSPHORYLATION; SIGNAL TRANSDUCTION; VAGUS NERVE STIMULATION; WESTERN BLOTTING;

ADENOSINE TRIPHOSPHATE; ANIMALS; APOPTOSIS; APOPTOSIS INDUCING FACTOR; BCL-ASSOCIATED DEATH PROTEIN; BLOTTING, WESTERN; BURNS; CYTOCHROMES C; CYTOSOL; DISEASE MODELS, ANIMAL; MALE; MICE; MICE, INBRED BALB C; MITOCHONDRIA, HEART; MITOCHONDRIAL SWELLING; MYOCARDIUM; MYOCYTES, CARDIAC; PHOSPHATIDYLINOSITOL 3-KINASES; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-AKT; PROTO-ONCOGENE PROTEINS C-BCL-2; SIGNAL TRANSDUCTION; VAGUS NERVE STIMULATION;

MURINAE; MUS;

EID: 84878355045     PISSN: 15821838     EISSN: None     Source Type: Journal    
DOI: 10.1111/jcmm.12049     Document Type: Article

References (25)

1. Singh V, Devgan L, Bhat S, et al. The pathogenesis of burn wound conversion. Ann Plast Surg. 2007; 59: 109-15.
2. Noel G, Guo X, Wang Q, et al. Postburn monocytes are the major producers of TNF-alpha in the heterogeneous splenic macrophage population. Shock. 2007; 27: 312-9.
3. Enkhbaatar P, Traber L, Traber D. Interleukin-1 in thermal injury: what is next? Crit Care Med. 2007; 35: 1212-3.
4. Jeschke MG, Chinkes DL, Finnerty CC, et al. Pathophysiologic response to severe burn injury. Ann Surg. 2008; 248: 387-401.
5. Jones SB, Muthu K, Shankar R, et al. Significance of the adrenal and sympathetic response to burn injury. In: Herndon DN, editor. Total burn care. Philadelphia, PA: Saunders Elsevier; 2007. pp. 343-60.
6. Costantini TW, Bansal V, Peterson CY, et al. Efferent vagal nerve stimulation attenuates gut barrier injury after burn: modulation of intestinal occluding expression. J Trauma. 2010; 68: 1349-54.
7. Gustafsson AB, Gottlieb RA. Mechanism of apoptosis in the heart. J Clin Immunol. 2003; 23: 447-59.
8. Katare RG, Ando M, Kakinuma Y, et al. Vagal nerve stimulation prevents reperfusion injury through inhibition of opening of mitochondrial permeability transition pore independent of the bradycardiac effect. J Thorac Cardiovasc Surg. 2009; 137: 223-31.
9. Costantini TW, Bansal V, Krzyzaniak M, et al. Vagal nerve stimulation protects against burn-induced intestinal injury through activation of enteric glia cells. Am J Physiol Gastrointest Liver Physiol. 2010; 299: 1308-18.
10. Downing SE, Lee JC. Effects of insulin on experimental catecholamine cardiomyopathy. Am J Pathol. 1978; 93: 339-52.
11. Iwata H, Goto H, Tanaka H, et al. Effect of maternal age on mitochondrial DNA copy number, ATP content and IVF outcome of bovine oocytes. Reprod Fertil Dev. 2011; 23: 424-32.
12. Honda HM, Ping P. Mitochondrial permeability transition in cardiac cell injury and death. Cardiovasc Drugs Ther. 2006; 20: 425-32.
13. Costantini TW, Krzyzaniak M, Cheadle GA, et al. Targeting α-7 nicotinic acetylcholine receptor in the enteric nervous system: a cholinergic agonist prevents gut barrier failure after severe burn injury. Am J Pathol. 2012; 181: 478-86.
14. Pavlov VA, Tracey KJ. The cholinergic anti-inflammatory pathway. Brain Behav Immunol. 2005; 19: 493-9.
15. + current in mouse atrial myocytes. J Biol Chem. 2002; 277: 27742-7.
16. + channel. J Membr Biol. 1999; 169: 55-64.
17. Yang B, Lin H, Xu C, et al. Choline produces cytoprotective effects against ischemic myocardial injuries: evidence for the role of cardiac M3 subtype muscarinic acetylcholine receptors. Cell Physiol Biochem. 2005; 16: 163-74.
18. + channels in canine atria with atrial fibrillation induced by experimental congestive heart failure. Cell Physiol Biochem. 2004; 14: 31-40.
19. 3 cholinoreceptors are present in pacemaker and working myocardium of murine heart. Pflugers Arch. 2012; 463: 523-9.
20. Miyamoto S, Rubio M, Sussman MA. Nuclear and mitochondrial signaling Akts in cardiomyocytes. Cardiovasc Res. 2009; 82: 272-85.
21. Matsui T, Tao J, del Monte F, et al. Akt activation preserves cardiac function and prevents injury after transient cardiac ischemia in vivo. Circulation. 2001; 104: 330-5.
22. del Peso L, Gonzalez-Garcia M, Page C, et al. Interleukin-3-induced phosphorylation of BAD through the protein kinase Akt. Science. 1997; 278: 687-9.
23. Ahmad N, Wang Y, Haider KH, et al. Cardiac protection by mitoKATP channels is dependent on Akt translocation from cytosol to mitochondria during late preconditioning. Am J Physiol Heart Circ Physiol. 2006; 290: 2402-8.
24. Imahashi K, Schneider MD, Steenbergen C, et al. Transgenic expression of Bcl-2 modulates energy metabolism, prevents cytosolic acidification during ischemia, and reduces ischemia/reperfusion injury. Circ Res. 2004; 95: 734-41.
25. Zhu L, Yu Y, Chua BH, et al. Regulation of sodium-calcium exchange and mitochondrial energetics by Bcl-2 in the heart of transgenic mice. J Mol Cell Cardiol. 2001; 33: 2135-44.