Myocardial ischemia/reperfusion causes VDAC phosphorylation which is reduced by cardioprotection with a p38 MAP kinase inhibitor

Proteomics

Volumn 7, Issue 24, 2007, Pages 4579-4588

  Schwertz, Hansjörg ^a   Carter, Justin M ^a   Abdudureheman, Mulati ^a   Russ, Martin ^a   Buerke, Ute ^a   Schlitt, Axel ^a   Müller Werdan, Ursula ^a   Prondzinsky, Roland ^a   Werdan, Karl ^a   Buerke, Michael ^a  

^a MARTIN LUTHER UNIVERSITY HALLE WITTENBERG   (Germany)

Author keywords

Apoptosis; Ischemia reperfusion injury; p38 mitogen activated protein kinases; Post translational protein modification; Voltage dependent anion channels

Indexed keywords

4 (4 FLUOROPHENYL) 2 (4 NITROPHENYL) 5 (4 PYRIDYL)IMIDAZOLE; HEAT SHOCK PROTEIN; MITOGEN ACTIVATED PROTEIN KINASE 1; VOLTAGE DEPENDENT ANION CHANNEL; VOLTAGE DEPENDENT ANION CHANNEL 1;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL SURVIVAL; CONTROLLED STUDY; ENZYME INHIBITION; HEART MUSCLE ISCHEMIA; HEART PROTECTION; MALE; NEUTROPHIL; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION;

ANIMALS; ANTIBODIES, PHOSPHO-SPECIFIC; CARDIOTONIC AGENTS; ELECTROPHORESIS, GEL, TWO-DIMENSIONAL; HEMODYNAMICS; IMIDAZOLES; MALE; MODELS, BIOLOGICAL; MYOCARDIAL REPERFUSION INJURY; MYOCARDIUM; NECROSIS; NEUTROPHILS; ORGAN SIZE; P38 MITOGEN-ACTIVATED PROTEIN KINASES; PHOSPHORYLATION; PROTEOME; PROTEOMICS; RABBITS; VOLTAGE-DEPENDENT ANION CHANNELS;

ORYCTOLAGUS CUNICULUS;

EID: 38049028598     PISSN: 16159853     EISSN: 16159861     Source Type: Journal    
DOI: 10.1002/pmic.200700734     Document Type: Article

References (33)

1. Ma, X. L., Kumar, S., Gao, F., Louden, C. S. et al., Inhibition of p38 mitogen-activated protein kinase decreases cardiomyocyte apoptosis and improves cardiac function after myocardial ischemia and reperfusion. Circulation 1999, 99, 1685-1691.
2. Takuma, K., Phuagphong, P., Lee, E., Mori, K. et al., Antiapoptotic effect of cGMP in cultured astrocytes: Inhibition by cGMP-dependent protein kinase of mitochondrial permeable transition pore. J. Biol. Chem. 2001, 276, 48093-48099.
3. Martin, J. L., Avkiran, M., Quinlan, R. A., Cohen, P., Marber, M. S., Antiischemic effects of SB 203580 are mediated through the inhibition of p38alpha mitogen-activated protein kinase: Evidence from ectopic expression of an inhibition-resistant kinase. Circ. Res. 2001, 89, 750-752.
4. Maulik, N., Yoshida, T., Zu, Y. L., Sato, M. et al., Ischemic preconditioning triggers tyrosine kinase signaling: A potential role for MAPKAP kinase 2. Am. J. Physiol. 1998, 275, H1857-1864.
5. Weinbrenner, C., Liu, G. S., Cohen, M. V., Downey, J. M., Phosphorylation of tyrosine 182 of p38 mitogen-activated protein kinase correlates with the protection of preconditioning in the rabbit heart. J. Mol. Cell. Cardiol. 1997, 29, 2383-2391.
6. Mackay, K., Mochly-Rosen, D., An inhibitor of p38 mitogen-activated protein kinase protects neonatal cardiac myocytes from ischemia. J. Biol. Chem. 1999, 274, 6272-6279.
7. Buerke, M., Schwertz, H., Seitz, W., Meyer, J., Darius, H., Novel small molecule inhibitor of C1s exerts cardioprotective effects in ischemia-reperfusion injury in rabbits. J. Immunol. 2001, 167, 5375-5380.
8. Schwertz, H., Langin, T., Platsch, H., Richert, J. et al., Two-dimensional analysis of myocardial protein expression following myocardial ischemia and reperfusion in rabbits. Proteomics 2002, 2, 988-995.
9. Bradley, P. P., Christensen, R. D., Rothstein, G., Cellular and extracellular myeloperoxidase in pyogenic inflammation. Blood 1982, 60, 618-622.
10. Buerke, M., Murohara, T., Lefer, A. M., Cardioprotective effects of a C1 esterase inhibitor in myocardial ischemia and reperfusion. Circulation 1995, 91, 393-402.
11. Popov, N., Schmitt, M., Schulzeck, S., Marthies, H., Reliable micromethod for determination of the protein content in tissue homogenates. Acta Biol. Med. Ger. 1975, 34, 1441-1446.
12. Heukeshoven, J., Dernick, R., Improved silver staining procedure for fast staining in PhastSystem Development Unit. I. Staining of sodium dodecyl sulfate gels. Electrophoresis 1988, 9, 28-32.
13. Yin, T., Sandhu, G., Wolfgang, C. D., Burrier, A. et al., Tissue-specific pattern of stress kinase activation in ischemic/reperfused heart and kidney. J. Biol. Chem. 1997, 272, 19943-19950.
14. Steenbergen, C., The role of p38 mitogen-activated protein kinase in myocardial ischemia/reperfusion injury; relationship to ischemic preconditioning. Basic Res. Cardiol. 2002, 97, 276-285.
15. Okada, T., Otani, H., Wu, Y., Kyoi, S. et al., Role of F-actin organization in p38 MAP kinase-mediated apoptosis and necrosis in neonatal rat cardiomyocytes subjected to simulated ischemia and reoxygenation. Am. J. Physiol. Heart Circ. Physiol. 2005, 289, H2310-H2318.
16. Gao, F., Yue, T. L., Shi, D. W., Christopher, T. A. et al., p38 MAPK inhibition reduces myocardial reperfusion injury via inhibition of endothelial adhesion molecule expression and blockade of PMN accumulation. Cardiovasc. Res. 2002, 53, 414-422.
17. Ashwell, J. D., The many paths to p38 mitogen-activated protein kinase activation in the immune system. Nat. Rev. Immunol. 2006, 6, 532-540.
18. Clerk, A., Sugden, P. H., Inflame my heart (by p38-MAPK). Circ. Res. 2006, 99, 455-458.
19. Sammut, I. A., Jayakumar, J., Latif, N., Rothery, S. et al., Heat stress contributes to the enhancement of cardiac mitochondrial complex activity. Am. J. Pathol. 2001, 158, 1821-1831.
20. Decker, R. S., Decker, M. L., Nakamura, S., Zhao, Y. S. et al., HSC73-tubulin complex formation during low-flow ischemia in the canine myocardium. Am. J. Physiol. Heart Circ. Physiol. 2002, 283, H1322-H1333.
21. Yaffe, M. B., Cantley, L. C., Signal transduction. Grabbing phosphoproteins. Nature 1999, 402, 30-31.
22. Liberatori, S., Canas, B., Tani, C., Bini, L. et al., Proteomic approach to the identification of voltage-dependent anion channel protein isoforms in guinea pig brain synaptosomes. Proteomics 2004, 4, 1335-1340.
23. Baines, C. P., Song, C. X., Zheng, Y. T., Wang, G. W. et al., Protein kinase Cepsilon interacts with and inhibits the permeability transition pore in cardiac mitochondria. Circ. Res. 2003, 92, 873-880.
24. Bera, A. K., Ghosh, S., Das, S., Mitochondrial VDAC can be phosphorylated by cyclic AMP-dependent protein kinase. Biochem. Biophys. Res. Commun. 1995, 209, 213-217.
25. Crompton, M., Barksby, E., Johnson, N., Capano, M., Mitochondrial intermembrane junctional complexes and their involvement in cell death. Biochimie 2002, 84, 143-152.
26. Suleiman, M. S., Halestrap, A. P., Griffiths, E. J., Mitochondria: A target for myocardial protection. Pharmacol. Ther. 2001, 89, 29-46.
27. Zamzami, N., Kroemer, G., The mitochondrion in apoptosis: How Pandora's box opens. Nat. Rev. Mol. Cell. Biol. 2001, 2, 67-71.
28. Halestrap, A. P., Clarke, S. J., Javadov, S. A., Mitochondrial permeability transition pore opening during myocardial reperfusion - a target for cardioprotection. Cardiovasc. Res. 2004, 61, 372-385.
29. Halestrap, A. P., Kerr, P. M., Javadov, S., Woodfield, K. Y., Elucidating the molecular mechanism of the permeability transition pore and its role in reperfusion injury of the heart. Biochim. Biophys. Acta 1998, 1366, 79-94.
30. Nazareth, W., Yafei, N., Crompton, M., Inhibition of anoxia-induced injury in heart myocytes by cyclosporin A. J. Mol. Cell. Cardiol. 1991, 23, 1351-1354.
31. Griffiths, E. J., Halestrap, A. P., Protection by Cyclosporin A of ischemia/reperfusion-induced damage in isolated rat hearts. J. Mol. Cell. Cardiol. 1993, 25, 1461-1469.
32. Halestrap, A. P., Connern, C. P., Griffiths, E. J., Kerr, P. M., Cyclosporin A binding to mitochondrial cyclophilin inhibits the permeability transition pore and protects hearts from ischaemia/reperfusion injury. Mol. Cell. Biochem. 1997, 174, 167-172.
33. Baines, C. P., Kaiser, R. A., Sheiko, T., Craigen, W. J., Molkentin, J. D., Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death. Nat. Cell. Biol. 2007, 9, 550-555.