The Molecular Mechanism Underlying Morphine-Induced Akt Activation: Roles of Protein Phosphatases and Reactive Oxygen Species

Cell Biochemistry and Biophysics

Volumn 61, Issue 2, 2011, Pages 303-311

  Xu, Jingman ^a   Tian, Wei ^a   Ma, Xiaolong ^b   Guo, Jing ^a   Shi, Qiuyan ^a   Jin, Yulan ^a   Xi, Jinkun ^a   Xu, Zhelong ^c  

^a HEBEI UNITED UNIVERSITY   (China)

^b Worker's Hospital   (China)

^c UNIVERSITY OF NORTH CAROLINA SCHOOL OF MEDICINE   (United States)

Author keywords

Akt; Morphine; Protein phosphatase 2A; Protein Ser Thr phosphatase; ROS

Indexed keywords

CARDIOTONIC AGENT; MORPHINE; PHOSPHATIDYLINOSITOL 3,4,5 TRISPHOSPHATE 3 PHOSPHATASE; PHOSPHOPROTEIN PHOSPHATASE 2; PROTEIN KINASE B; REACTIVE OXYGEN METABOLITE;

ANIMAL; ARTICLE; CELL LINE; CELL SURVIVAL; CYTOLOGY; DOSE RESPONSE; DRUG EFFECT; ENZYME ACTIVATION; METABOLISM; MYOBLAST; PHOSPHORYLATION; RAT;

ANIMALS; CARDIOTONIC AGENTS; CELL LINE; CELL SURVIVAL; DOSE-RESPONSE RELATIONSHIP, DRUG; ENZYME ACTIVATION; MORPHINE; MYOBLASTS, CARDIAC; PHOSPHORYLATION; PROTEIN PHOSPHATASE 2; PROTO-ONCOGENE PROTEINS C-AKT; PTEN PHOSPHOHYDROLASE; RATS; REACTIVE OXYGEN SPECIES;

EID: 80955151555     PISSN: 10859195     EISSN: None     Source Type: Journal    
DOI: 10.1007/s12013-011-9213-5     Document Type: Article

References (45)

1. Gross, G. J. (2003). Role of opioids in acute and delayed preconditioning. Journal of Molecular and Cellular Cardiology, 35, 709-718.
2. Schultz, J. E., Hsu, A. K., & Gross, G. J. (1998). Ischemic preconditioning in the intact rat heart is mediated by delta1- but not mu- or kappa-opioid receptors. Circulation, 97, 1282-1289.
3. Schultz, J. J., Hsu, A. K., Nagase, H., & Gross, G. J. (1998). TAN-67, a delta-opioid receptor agonist, reduces infarct size via activation of Gi/o proteins and Katp channels. American Journal of Physiology, 274, H909-H914.
4. Huh, J., Gross, G. J., Nagase, H., & BT, L. (2001). Protection of cardiac myocytes via delta(1)-opioid receptors, protein kinase C, and mitochondrial K(ATP) channels. American Journal of Physiology Heart and Circulatory Physiology, 280, H377-H383.
5. Wu, S., Li, H.-Y., & Wong, T. M. (1999). Cardioprotection of preconditioning by metabolic inhibition in the rat ventricular myocyte. Circulation Research, 84, 1388-1395.
6. Wang, G. Y., Wu, S., Pei, J. M., Yu, X. C., & Wong, T. M. (2001). Kappa- but not delta-opioid receptors mediate effects of ischemic preconditioning on both infarct and arrhythmia in rats. American Journal of Physiology Heart and Circulatory Physiology, 280, H384-H391.
7. Miki, T., Cohen, M. V., & Downey, J. M. (1998). Opioid receptor contributes to ischemic preconditioning through protein kinase C activation in rabbits. Molecular and Cellular Biochemistry, 186, 3-12.
8. Fryer, R. M., Wang, Y., Hsu, A. K., & Gross, G. J. (2001). Essential activation of PKC-delta in opioid-initiated cardioprotection. American Journal of Physiology Heart and Circulatory Physiology, 280, H1346-H1353.
9. Liang, B. T., & Gross, G. J. (1999). Direct preconditioning of cardiac myocytes via opioid receptors and KATP channels. Circulation Research, 84, 1396-1400.
10. Fryer, R. M., Schultz, J. E. J., Hsu, A. K., & Gross, G. J. (1998). Pretreatment with tyrosine kinase inhibitors partially attenuates ischemic preconditioning in rat hearts. American Journal of Physiology, 275, H2009-H2015.
11. Fryer, R. M., Pratt, P. F., Hsu, A. K., & Gross, G. J. (2001). Differential activation of extracellular signal regulated kinase isoforms in preconditioning and opioid-induced cardioprotection. Journal of Pharmacology and Experimental Therapeutics, 296, 642-649.
12. Fryer, R. M., Hsu, A. K., & Gross, G. J. (2001). ERK and p38 MAP kinase activation are components of opioid-induced delayed cardioprotection. Basic Research in Cardiology, 96, 136-142.
13. Gross, E. R., Hsu, A. K., & Gross, G. J. (2006). The JAK/STAT pathway is essential for opioid-induced cardioprotection: JAK2 as a mediator of STAT3, Akt, and GSK-3beta. American Journal of Physiology, 291, H827-H834.
14. Peart, J. N., & Gross, G. J. (2006). Cardioprotective effects of acute and chronic opioid treatment are mediated via different signaling pathways. American Journal of Physiology, 291, H1746-H1753.
15. Gross, E. R., Hsu, A. K., & Gross, G. J. (2007). Diabetes abolishes morphine-induced cardioprotection via multiple pathways upstream of glycogen synthase kinase-3beta. Diabetes, 56, 127-136.
16. Cohen, M. V., Philipp, S., Krieg, T., Cui, L., Kuno, A., Solodushko, V., et al. (2007). Preconditioning-mimetics bradykinin and DADLE activate PI3-kinase through divergent pathways. Journal of Molecular and Cellular Cardiology, 42, 842-851.
17. Forster, K., Kuno, A., Solenkova, N., Felix, S. B., & Krieg, T. (2007). The {delta}-opioid receptor agonist DADLE at reperfusion protects the heart through activation of pro-survival kinases via EGF receptor transactivation. American Journal of Physiology, 293, H1604-H1608.
18. Gross, E. R., Hsu, A. K., & Gross, G. J. (2004). Opioid-induced cardioprotection occurs via glycogen synthase kinase β inhibition during reperfusion in intact rat hearts. Circulation Research, 94, 960-966.
19. Matsui, T., & Rosenzweig, A. (2005). Convergent signal transduction pathways controlling cardiomyocyte survival and function: the role of PI 3-kinase and Akt. Journal of Molecular and Cellular Cardiology, 38, 63-71.
20. Brazil, D. P., & Hemmings, B. A. (2001). Ten years of protein kinase B signalling: a hard Akt to follow. Trends in Biochemical Sciences, 26, 657-664.
21. Miyamoto, S., Murphy, A., & Brown, J. (2009). Akt mediated mitochondrial protection in the heart: metabolic and survival pathways to the rescue. Journal of Bioenergetics and Biomembranes, 41, 169-180.
22. Mocanu, M. M., & Yellon, D. M. (2007). PTEN, the Achilles' heel of myocardial ischaemia/reperfusion injury? British Journal of Pharmacology, 150, 833-838.
23. Millward, T. A., Zolnierowicz, S., & Hemmings, B. A. (1999). Regulation of protein kinase cascades by protein phosphatase 2A. Trends in Biochemical Sciences, 24, 186-191.
24. 2. The Journal of Biological Chemistry, 277, 20336-20342.
25. Hausenloy, D. J., & Yellon, D. M. (2006). Survival kinases in ischemic preconditioning and postconditioning. Cardiovascular Research, 70, 240-253.
26. Jang, Y. G., Xi, J. K., Wang, H. H., Mueller, R. A., Norfleet, E. A., & Xu, Z. L. (2008). Postconditioning prevents reperfusion injury by activating delta-opioid receptors. Anesthesiology, 108, 243-250.
27. Cai, Z., & Semenza, G. L. (2005). PTEN activity is modulated during ischemia and reperfusion: Involvement in the induction and decay of preconditioning. Circulation Research, 97, 1351-1359.
28. Mensah, K., Mocanu, M. M., & Yellon, D. M. (2005). Failure to protect the myocardium against ischemia/reperfusion injury after chronic atorvastatin treatment is recaptured by acute atorvastatin treatment: A potential role for phosphatase and tensin homolog deleted on chromosome ten? Journal of the American College of Cardiology, 45, 1287-1291.
29. Gericke, A., Munson, M., & Ross, A. H. (2006). Regulation of the PTEN phosphatase. Gene, 374, 1-9.
30. Cohen, M. V., Yang, X.-M., Liu, G. S., Heusch, G., & Downey, J. M. (2001). Acetylcholine, bradykinin, opioids, and phenylephrine, but not adenosine, trigger preconditioning by generating free radicals and opening mitochondrial K(ATP) channels. Circulation Research, 89, 273-278.
31. Vanhaesebroeck, B., & Alessi, D. R. (2000). The PI3K-PDK1 connection: more than just a road to PKB. Biochemical Journal, 346, 561-576.
32. Barthel, A., & Klotz, L. O. (2005). Phosphoinositide 3-kinase signaling in the cellular response to oxidative stress. Biological Chemistry, 386, 207-216.
33. Cohen, P. T. W. (1997). Novel protein serine/threonine phosphatases: Variety is the spice of life. Trends in Biochemical Sciences, 22, 245-251.
34. Weinbrenner, C., Baines, C. P., Liu, G.-S., Armstrong, S. C., Ganote, C. E., Walsh, A. H., et al. (1998). Fostriecin, an inhibitor of protein phosphatase 2A, limits myocardial infarct size even when administered after onset of ischemia. Circulation, 98, 899-905.
35. Armstrong, S. C., & Ganote, C. E. (1992). Effects of the protein phosphatase inhibitors okadaic acid and calyculin A on metabolically inhibited and ischaemic isolated myocytes. Journal of Molecular and Cellular Cardiology, 24, 869-884.
36. Lee, S., Chanoit, G., McIntosh, R., Zvara, D. A., & Xu, Z. L. (2009). Molecular mechanism underlying Akt activation in zinc-induced cardioprotection. American Journal of Physiology, 297, H569-H575.
37. Chen, L., Liu, L., & Huang, S. (2008). Cadmium activates the mitogen-activated protein kinase (MAPK) pathway via induction of reactive oxygen species and inhibition of protein phosphatases 2A and 5. Free Radical Biology and Medicine, 45, 1035-1044.
38. Whisler, R. L., Goyette, M. A., Grants, I. S., & Newhouse, Y. G. (1995). Sublethal levels of oxidant stress stimulate multiple serine/threonine kinases and suppress protein phosphatases in Jurkat T cells. Archives of Biochemistry and Biophysics, 319, 23-35.
39. Downey, J., Davis, A., & Cohen, M. (2007). Signaling pathways in ischemic preconditioning. Heart Failure Reviews, 12, 181-188.
40. Fryer, R. M., Schultz, J. E. J., Hsu, A. K., & Gross, G. J. (1999). Importance of PKC and tyrosine kinase in single or multiple cycles of preconditioning in rat hearts. American Journal of Physiology, 276, H1229-H1235.
41. Yang, X., Cohen, M., & Downey, J. (2010). Mechanism of cardioprotection by early ischemic preconditioning. Cardiovascular Drugs and Therapy, 24, 225-234.
42. Yue, Y., Qin, Q., Cohen, M. V., Downey, J. M., & Critz, S. D. (2002). The relative order of mK(ATP) channels, free radicals and p38 MAPK in preconditioning's protective pathway in rat heart. Cardiovascular Research, 55, 681-689.
43. Oldenburg, O., Qin, Q., Sharma, A., Cohen, M., Downey, J., & Benoit, J. (2002). Acetylcholine leads to free radical production dependent on K(ATP) channels, G(i) proteins, phosphatidylinositol 3-kinase and tyrosine kinase. Cardiovascular Research, 55, 544-552.
44. Oldenburg, O., Qin, Q., Krieg, T., Yang, X. M., Philipp, S., Critz, S. D., et al. (2003). Bradykinin induces mitochondrial ROS generation via NO, cGMP, PKG, and mKATP channel opening and leads to cardioprotection. American Journal of Physiology Heart and Circulatory Physiology, 286, H468-H476.
45. McPherson, B. C., & Yao, Z. (2001). Morphine mimics preconditioning via free radical signals and mitochondrial KATP channels in myocytes. Circulation, 103, 290-295.