Interactions of GSK-3β with mitochondrial permeability transition pore modulators during preconditioning: Age-associated differences

Journals of Gerontology - Series A Biological Sciences and Medical Sciences

Volumn 68, Issue 4, 2013, Pages 395-403

  Zhu, Jiang ^a,b   Rebecchi, Mario J ^a   Glass, Peter S A ^a   Brink, Peter R ^c   Liu, Lixin ^a  

^a STONY BROOK UNIVERSITY   (United States)

^b THE SECOND AFFILIATED HOSPITAL OF SOOCHOW UNIVERSITY   (China)

^c STONY BROOK UNIVERSITY   (United States)

Author keywords

Aging; GSK 3 ; mPTP; Preconditioning

Indexed keywords

ADENINE NUCLEOTIDE TRANSLOCASE; CARRIER PROTEIN; CYCLOPHILIN; CYCLOPHILIN D; GLYCOGEN SYNTHASE KINASE 3; GLYCOGEN SYNTHASE KINASE 3 BETA; MITOCHONDRIAL PERMEABILITY TRANSITION PORE; VOLTAGE DEPENDENT ANION CHANNEL;

AGE; ANIMAL; ANIMAL MODEL; ARTICLE; CELL AGING; FISCHER 344 RAT; HEART INFARCTION PREVENTION; HEART MITOCHONDRION; HEART MUSCLE CELL; IMMUNOPRECIPITATION; MALE; METABOLISM; METHODOLOGY; OXIDATIVE STRESS; RAT;

AGE FACTORS; ANIMALS; CELL AGING; CYCLOPHILINS; GLYCOGEN SYNTHASE KINASE 3; IMMUNOPRECIPITATION; ISCHEMIC PRECONDITIONING, MYOCARDIAL; MALE; MITOCHONDRIA, HEART; MITOCHONDRIAL ADP, ATP TRANSLOCASES; MITOCHONDRIAL MEMBRANE TRANSPORT PROTEINS; MODELS, ANIMAL; MYOCYTES, CARDIAC; OXIDATIVE STRESS; RATS; RATS, INBRED F344; VOLTAGE-DEPENDENT ANION CHANNELS;

MLCS; MLOWN;

EID: 84875164497     PISSN: 10795006     EISSN: 1758535X     Source Type: Journal    
DOI: 10.1093/gerona/gls205     Document Type: Article

References (34)

1. Hunter DR, Haworth RA. The Ca2+-induced membrane transition in mitochondria. I. The protective mechanisms. Arch Biochem Biophys. 1979;195:453-459.
2. Green DR, Reed JC. Mitochondria and apoptosis. Science. 1998;281:1309-1312.
3. Halestrap AP, Brenner C. The adenine nucleotide translocase: a central component of the mitochondrial permeability transition pore and key player in cell death. Curr Med Chem. 2003;10:1507-1525.
4. Di Lisa F, Carpi A, Giorgio V, Bernardi P. The mitochondrial permeability transition pore and cyclophilin D in cardioprotection. Biochim Biophys Acta. 2011;1813:1316-1322.
5. Miura T, Nishihara M, Miki T. Drug development targeting the glycogen synthase kinase-3beta (GSK-3beta)-mediated signal transduction pathway: role of GSK-3beta in myocardial protection against ischemia/reperfusion injury. J Pharmacol Sci. 2009;109:162-167.
6. Jope RS, Yuskaitis CJ, Beurel E. Glycogen synthase kinase-3 (GSK3): inflammation, diseases, and therapeutics. Neurochem Res. 2007;32:577-595.
7. Cohen P, Goedert M. GSK3 inhibitors: development and therapeutic potential. Nat Rev Drug Discov. 2004;3:479-487.
8. Gross ER, Hsu AK, Gross GJ. Opioid-induced cardioprotection occurs via glycogen synthase kinase beta inhibition during reperfusion in intact rat hearts. Circ Res. 2004;94:960-966.
9. Tong H, Imahashi K, Steenbergen C, Murphy E. Phosphorylation of glycogen synthase kinase-3beta during preconditioning through a phosphatidylinositol-3- kinase-dependent pathway is cardioprotective. Circ Res. 2002;90:377-379.
10. Liu L, Zhu J, Brink PR, Glass PS, Rebecchi MJ. Age-associated differences in the inhibition of mitochondrial permeability transition pore opening by cyclosporine A. Acta Anaesthesiol Scand. 2011;55:622-630.
11. Zhu J, Rebecchi MJ, Glass PS, Brink PR, Liu L. Cardioprotection of the aged rat heart by GSK-3beta inhibitor is attenuated: age-related changes in mitochondrial permeability transition pore modulation. Am J Physiol Heart Circ Physiol. 2011;300:H922-H930.
12. Zhu J, Rebecchi MJ, Tan M, Glass PS, Brink PR, Liu L. Age-associated differences in activation of Akt/GSK-3beta signaling pathways and inhibition of mitochondrial permeability transition pore opening in the rat heart. J Gerontol A Biol Sci Med Sci. 2010;65:611-619.
13. Liu L, Zhu J, Glass PS, Brink PR, Rampil IJ, Rebecchi MJ. Ageassociated changes in cardiac gene expression after preconditioning. Anesthesiology. 2009;111:1052-1064.
14. Nguyen LT, Rebecchi MJ, Moore LC, Glass PS, Brink PR, Liu L. Attenuation of isoflurane-induced preconditioning and reactive oxygen species production in the senescent rat heart. Anesth Analg. 2008;107:776-782.
15. Hirata N, Shim YH, Pravdic D, et al. Isoflurane differentially modulates mitochondrial reactive oxygen species production via forward versus reverse electron transport flow: implications for preconditioning. Anesthesiology. 2011;115:531-540.
16. Diaz RJ, Zobel C, Cho HC, et al. Selective inhibition of inward rectifier K+ channels (Kir2.1 or Kir2.2) abolishes protection by ischemic preconditioning in rabbit ventricular cardiomyocytes. Circ Res. 2004;95:325-332.
17. O'Brien JD, Ferguson JH, Howlett SE. Effects of ischemia and reperfusion on isolated ventricular myocytes from young adult and aged Fischer 344 rat hearts. Am J Physiol Heart Circ Physiol. 2008;294:H2174-H2183.
18. Fraticelli A, Josephson R, Danziger R, Lakatta E, Spurgeon H. Morphological and contractile characteristics of rat cardiac myocytes from maturation to senescence. Am J Physiol. 1989;257:H259-H265.
19. Pravdic D, Sedlic F, Mio Y, Vladic N, Bienengraeber M, Bosnjak ZJ. Anesthetic-induced preconditioning delays opening of mitochondrial permeability transition pore via protein Kinase C-epsilon-mediated pathway. Anesthesiology. 2009;111:267-274.
20. Hausenloy DJ, Ong SB, Yellon DM. The mitochondrial permeability transition pore as a target for preconditioning and postconditioning. Basic Res Cardiol. 2009;104:189-202.
21. Miura T, Tanno M, Sato T. Mitochondrial kinase signalling pathways in myocardial protection from ischaemia/reperfusion-induced necrosis. Cardiovasc Res. 2010;88:7-15.
22. Di Lisa F, Bernardi P. Mitochondria and ischemia-reperfusion injury of the heart: fixing a hole. Cardiovasc Res. 2006;70:191-199.
23. Halestrap AP, Clarke SJ, Javadov SA. Mitochondrial permeability transition pore opening during myocardial reperfusion-a target for cardioprotection. Cardiovasc Res. 2004;61:372-385.
24. Boengler K, Schulz R, Heusch G. Loss of cardioprotection with ageing. Cardiovasc Res. 2009;83:247-261.
25. Lesnefsky EJ, Moghaddas S, Tandler B, Kerner J, Hoppel CL. Mitochondrial dysfunction in cardiac disease: ischemia-reperfusion, aging, and heart failure. J Mol Cell Cardiol. 2001;33:1065-1089.
26. Das S, Wong R, Rajapakse N, Murphy E, Steenbergen C. Glycogen synthase kinase 3 inhibition slows mitochondrial adenine nucleotide transport and regulates voltage-dependent anion channel phosphorylation. Circ Res. 2008;103:983-991.
27. Park SS, Zhao H, Jang Y, Mueller RA, Xu Z. N6-(3-iodobenzyl)-adenosine- 5'-N-methylcarboxamide confers cardioprotection at reperfusion by inhibiting mitochondrial permeability transition pore opening via glycogen synthase kinase 3 beta. J Pharmacol Exp Ther. 2006;318:124-131.
28. Clarke SJ, McStay GP, Halestrap AP. Sanglifehrin A acts as a potent inhibitor of the mitochondrial permeability transition and reperfusion injury of the heart by binding to cyclophilin-D at a different site from cyclosporin A. J Biol Chem. 2002;277:34793-34799.
29. Li Y, Johnson N, Capano M, Edwards M, Crompton M. Cyclophilin-D promotes the mitochondrial permeability transition but has opposite effects on apoptosis and necrosis. Biochem J. 2004;383:101-109.
30. Khaspekov L, Friberg H, Halestrap A, Viktorov I, Wieloch T. Cyclosporin A and its nonimmunosuppressive analogue N-Me-Val-4-cyclosporin A mitigate glucose/oxygen deprivation-induced damage to rat cultured hippocampal neurons. Eur J Neurosci. 1999;11:3194-3198.
31. Nakagawa T, Shimizu S, Watanabe T, et al. Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death. Nature. 2005;434:652-658.
32. Baines CP, Kaiser RA, Purcell NH, et al. Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death. Nature. 2005;434:658-662.
33. Schinzel AC, Takeuchi O, Huang Z, et al. Cyclophilin D is a component of mitochondrial permeability transition and mediates neuronal cell death after focal cerebral ischemia. Proc Natl Acad Sci USA. 2005;102:12005-12010.
34. Baines CP, Kaiser RA, Sheiko T, Craigen WJ, Molkentin JD. Voltagedependent anion channels are dispensable for mitochondrial-dependent cell death. Nat Cell Biol. 2007;9:550-555.