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Review

Sarcoplasmic reticulum and cardiac oxidative stress: an emerging target for heart disease

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Pages 205-217 | Published online: 25 Feb 2005

Bibliography

  • DHALLA NS, TEMSAH RM, NETTICADAN T: Role of oxidative stress in cardiovascular diseases. J. Hypertens. (2000) 18 (6):655–673.
  • ••A thorough review of oxidative stress.
  • FABIATO A: Calcium-induced release of calcium from the cardiac sarcoplasmic reticulum. Am. J Physiol. (1983) 245(1):C1–14.
  • MACLENNAN DH, WONG PT: Isolation of a calcium-sequestering protein from sarcoplasmic reticulum. Proc. Natl. Acad. ScL USA (1971) 68(6):1231–1235.
  • JORGENSEN AO, SHEN AC, DALY P, MACLENNAN DH: Localization of Ca2+ Mg2+-ATPase of the sarcoplasmic reticulum in adult rat papillary muscle. J Cell Biol. (1982) 93(3):883–892.
  • BASSANI JVV, BASSANI RA, BERS DM: Relaxation in rabbit and rat cardiac cells: species-dependent differences in cellular mechanisms. J. Physiol (fond) (1994) 476 (2):279–293.
  • BERS DM: Ca transport during contraction and relaxa-tion in mammalian ventricular muscle. In: Alterations of excitation-contraction coupling in the failing human heart. Hasenfuss G, Just H (Eds.), Springer-Verlag, New York (1998):1–16.
  • BALTAS LG, KARCZEWSKI P, KRAUSE EG: The cardiac sarcoplasmic reticulum phospholamban kinase is a distinct delta-CaM kinase isozyme. FEBS Lett. (1995) 373 (1):71–75.
  • KRANIAS EG, SCHVVARTZ A, JUNGMANN RA: Characteri-zation of cyclic 3',5'-amp-dependent protein kinase in sarcoplasmic reticulum and cytosol of canine myocar-dium. Biochim. Biophys. Acta (1982) 709(0:28–37.
  • HAWKINS C, XU A, NARAYANAN N: Sarcoplasmic reticulum calcium pump in cardiac and slow twitch skeletal muscle but not fast twitch skeletal muscle undergoes phosphorylation by endogenous and exogenous Ca2+/calmodulin-dependent protein kinase. Characterization of optimal conditions for calcium pump phosphorylation. J. Biol. Chem. (1994) 269 (49):31198–31206.
  • LE PEUCH CJ, HAIECH J, DEMAILLE JG: Concerted regula- tion of cardiac sarcoplasmic reticulum calcium transport by cyclic adenosine monophosphate dependent and calcium-calmodulin-dependent phosphorylations. Biochemistry (1979) 18 (23):5150–5157.
  • XU A, HAWKINS C, NARAYANAN N: Phosphorylation and activation of the Ca2±-pumping ATPase of cardiac sarcoplasmic reticulum by Ca2±/calmodulin-dependent protein kinase. J. Biol. Chem. (1993) 268 (12):8394–8397.
  • LINDEMANN JP, WATANABE AM: Muscarinic cholinergic inhibition of 13-adrenergic stimulation of phospholamban phosphorylation and Ca2+ transport in guinea pig ventricles. J. Biol. Chem. (1985) 260(2013122–13129.
  • SUZUKI T, WANG JH: Stimulation of bovine cardiac sarcoplasmic reticulum Ca2+ pump and blocking of phospholamban phosphorylation and dephosphory-lation by a phospholamban monoclonal antibody. J Biol. Chem. (1986) 261 (15):7018–7023.
  • SASAKI T, INUI M, KIMURA Y, KUZUYA T, TADA M: Molecular mechanism of regulation of Ca2+ pump ATPase by phospholamban in cardiac sarcoplasmic reticulum. Effects of synthetic ph osph olamban peptides on Ca2+ pump ATPase. J. Biol. Chem. (1992) 267 (3):1674–1679.
  • TADA M, KIRCHBERGER MA: Regulation of calcium transport by cyclic AMP. A proposed mechanism for the 13-adrenergic control of myocardial contractility. Acta Cardiol (1975) 30 (4):231–237.
  • WEGENER AD, SIMMERMAN HK, LINDEMANN JP, JONES LR: Phospholamban phosphorylation in intact ventri-cles.Phosphorylation of serine 16 and threonine 17 in response to 13-adrenergic stimulation. J. Biol. Chem. (1989) 264 (19):11468–11474.
  • KRANIAS EG: Regulation of calcium transport by protein phosphatase activity associated with cardiac sarcoplasmic reticulum. J. Biol. Chem. (1985) 260 (2011006–11010.
  • TOYOFUKU T, CUROTTO KURZYDLOWSKI K, NARAYANAN N, MACLENNAN DH: Identification of Ser38 as the site in cardiac sarcoplasmic reticulum Ca2+-ATPase that is phosphorylated by Ca2+/calmodu-lin- dependent protein kinase. j Biol. Chem. (1994) 269 (42):26492–26496.
  • TAKASAGO T, IMAGAWA T, FURUKAWA K, OGURUSU T, SHIGEKAWA M: Regulation of the cardiac ryanodine receptor by protein kinase-dependent phosphoryla-tion. Biochem. (Tokyo) (1991) 109(0:163–170.
  • WITCHER DR, KOVACS RJ, SCHULMAN H, CEFALI DC, JONES LR: Unique phosphorylation site on the cardiac ryanodine receptor regulates calcium channel activity. J Biol. Chem. (1991) 266(17):11144–11152.
  • DHALLA NS, PIERCE GN, PANAGIA V, SINGAL PK, BEAMISH RE: Calcium movements in relation to heart function. Basic Res. Cardiol. (1982) 77(2):117–139.
  • DHALLA NS, TEMSAH RM, NETTICADAN T, SANDHU MS: Intracellular calcium overload: a critical factor in ischemia/reperfusion injury. In: Heart Physiology and Pathophysiology. Sperelakis N et al. (Eds.), Academic Press, San Diego (2000):949–965.
  • ••A thorough review of Ca2+-over1oad.
  • FLECKENSTEIN A: Specific inhibitors and promoters of calcium action in the excitation-contraction coupling of heart muscle and their role in the prevention or production of myocardial lesions. In: Calcium and the Heart. Harris P, Opie L (Eds.), Academic Press, New York (1970:135–188.
  • TANI M: Mechanisms of Ca2+-overload in reperfused ischemic myocardium. Annu. Rev. Physiol. (1990) 52:543–559.
  • MARBAN E, KORETSUNE Y, CORRETTI M, CHACKO VP,KUSUOKA H: Calcium and its role in myocardial cell injury during ischemia and reperfusion. Circulation (1989) 80 (Suppl. 6):IV17–22.
  • SCHUMACHER CA, BAARTSCHEER A, CORONEL R, FIOLET JW: Energy-dependent transport of calcium to the extracellular space during acute ischemia of the rat heart. J. Mot. Cell Cardiol. (1998) 30(8):1631–1642.
  • VAN ECHTELD CJ, KIRKELS JH, EIJGELSHOVEN MH, VAN DER MP, RUIGROK TJ: Intracellular sodium during ischemia and calcium-free perfusion: a 23Na NMR study. J. Mot. Cell Cardiol. (1991) 23(3):297–307.
  • MARBAN E, KORETSUNE Y, CORRETTI M, CHACKO VP, KUSUOKA H: Calcium and its role in myocardial cell injury during ischemia and reperfusion. Circulation (1989) 80 (Suppl. 6):IV17–22.
  • WU J, CORR PB: Influence of long-chain acylcarnitines on voltage-dependent calcium current in adult ventricular myocytes. Am. J Physiol. (1992) 2 63 (2 Pt 2):H410–7.
  • DHALLA NS, ELIMBAN V, RUPP H: Paradoxical role of lipid metabolism in heart function and dysfunction. Mol. Cell Biochem. (1992) 11 6 (1–2):3–9.
  • MUKHERJEE A, WONG TM, BUJA LM, LEFKOWITZ RJ, WILLERSON JT: 13-adrenergic and muscarinic cholinergic receptors in canine myocardium. Effects of ischemia. j Clin. Invest. (1979) 64 (5):1423–1428.
  • YOSHIDA Y, SHIGA T, IMAI S: Degradation of sarcoplasmic reticulum calcium-pumping ATPase in ischemic-reperfused myocardium: role of calcium-activated neutral protease. Basic Res. Cardiol. (1990) 85(5)495–507.
  • RARDON DP, CEFALI DC, MITCHELL RD et al.: Digestionof cardiac and skeletal muscle junctional sarcoplasmic reticulum vesicles with calpain II. Effects on the Ca2+ release channel. Circ. Res. (1990) 67(0:84–96.
  • GESCHMAN R, GILBERT DL, NYE SW, SWEYER P, FERRARIR: Oxygen poisoning and X-irradiation: a mechanism in common. Science (1954)
  • FRIDOVICH I: Superoxide dismutases. Adv. Enzymol. Relat Areas Mol. Biol. (1986) 58:61–97.
  • ENGLER RL, SCHMID-SCHONBEIN GW, PAVELEC RS: Leukocyte capillary plugging in myocardial ischemia and reperfusion in the dog. Am. J. Pathol. (1983) 111 (1):98–111.
  • HAMMOND B, KONTOS HA, HESS ML: Oxygen radicals in the adult respiratory distress syndrome, in myocar-dial ischemia and reperfusion injury, and in cerebral vascular damage. Can. J. Physiol. Pharmacol. (1985) 63(3):173–187.
  • KALRA J, CHAUDHARY AK, PRASAD K: Role of oxygen free radicals and pH on the release of cardiac lysosomal enzymes. J. Mol. Cell Cardiol. (1989) 21 (11):1125–1136.
  • GIROTTI AW: Mechanisms of lipid peroxidation. J Free Radic. Biol. Med. (1985) 1(2):87–95.
  • GRINNA LS: Age related changes in the lipids of the microsomal and the mitochondrial membranes of rat liver and kidney. Mech. Ageing Dev. (1977) 6 (3):197–205.
  • HEARSE DJ: Reperfusion-induced injury: a possible role for oxidant stress and its manipulation. Cardio-vasc. Drugs Ther. (1991) 5 (Suppl. 2):225–235.
  • NETTICADAN T, TEMSAH R, OSADA M, DHALLA NS: Status of Ca2±/calmodulin protein kinase phosphory-lation of cardiac SR proteins in ischemia-reperfusion. Am. J. Physic)]. (1999) 277(3 Pt 1):C384–C391.
  • TEMSAH RM, NETTICADAN T, CHAPMAN D eta].: Altera-tions in sarcoplasmic reticulum function and gene expression in ischemic-reperfused rat heart. Am. J Physiol. (1999) 277(2 Pt 2):H584–H594.
  • ZUCCHI R, RONCA-TESTONI S, YU G et al.: Postischemic changes in cardiac sarcoplasmic reticulum Ca2+ channels. A possible mechanism of ischemic precon-ditioning. Circ. Res. (1995) 76 (6) :1049–1056.
  • XU KY, ZWEIER JL, BECKER LC: Hydroxyl radical inhibits sarcoplasmic reticulum Ca2+-ATPase function by direct attack on the ATP binding site. Circ. Res. (1997) 80 (1):76–81.
  • KUKREJA RC, HESS ML: The oxygen free radical system: from equations through membrane-protein interac-tions to cardiovascular injury and protection. Cardio-vasc. Res. (1992) 2 6 (7):641–655.
  • STOYANOVSKY D, MURPHY T, ANNO PR, KIM YM, SALAMA G: Nitric oxide activates skeletal and cardiac ryanodine receptors. Cell Calcium (1997) 21(0:19–29.
  • FAVERO TG, ZABLE AC, ABRAMSON JJ: Hydrogen peroxide stimulates the Ca2+ release channel from skeletal muscle sarcoplasmic reticulum. J Biol. Chem. (1995) 270(43):25557–25563.
  • GWATHMEY JK, COPELAS L, MACKINNON R et al.: Abnormal intracellular calcium handling in myocar-dium from patients with end-stage heart failure. Circ. Res. (1987) 61 (1):70–76.
  • GWATHMEY JK, HADAR RJ: Relation between steady-state force and intracellular ra21 in intact human myocardium. Index of myofibrillar responsiveness to Ca2±. Circulation (1990) 82(4):1266–1278.
  • MORGAN JP, ERNY RE, ALLEN PD, GROSSMAN W, GWATHMEY JK: Abnormal intracellular calcium handling, a major cause of systolic and diastolic dysfunction in ventricular myocardium from patients with heart failure. Circulation (1990) 81 (Suppl. 2):III21–11132.
  • GWATHMEY JK, MORGAN JP: Sarcoplasmic reticulum calcium mobilization in right ventricular pressure-overload hypertrophy in the ferret: relationships to diastolic dysfunction and a negative treppe. Pflugers Arch. (1993) 422 (6):599–608.
  • SCHMIDT U, HADAR RJ, HELM PA et al.: Contribution of abnormal sarcoplasmic reticulum ATPase activity to systolic and diastolic dysfunction in human heart failure. J. Mol Cell Cardiol. (1998) 3 0 (10) :1929–1937.
  • NETTICADAN T, TEMSAH RM, KAWABATA K, DHALLA NS: Sarcoplasmic reticulum Ca2+/Calmodulin-dependent protein kinase is altered in heart failure. Circ. Res. (2000) 86 (5) 596–605.
  • HADAR RJ, KANG JX, GWATHMEY JK, ROSENZWEIG A: Physiological effects of adenoviral gene transfer of sarcoplasmic reticulum calcium ATPase in isolated rat myocytes. Circulation (1997) 95 (2):423–429.
  • MEYER M, BLUHM WF, HE H et al.: Phospholamban-to-SERCA2 ratio controls the force-frequency relation-ship. Am. J. Physic]. (1999) 276(3 Pt 2):H779–H785.
  • DEPRE C, DAVIES PJ, TAEGTMEYER H: Transcriptional adaptation of the heart to mechanical unloading. Am../ Cardiol. (1999) 83 (12A):58H–63H.
  • PETERS DG, MITCHELL-FELTON H, KANDARIAN SC: Unloading induces transcriptional activation of the sarco(endo)plasmic reticulum Ca2+-ATPase 1 gene in muscle. Am. J. Physiol (1999) 276(5 Pt 1):C1218–C1225.
  • BARTLING B, MILTING H, SCHUMANN H et al.: Myocar-dial gene expression of regulators of myocyte apoptosis and myocyte calcium homeostasis during hemodynamic unloading by ventricular assist devices in patients with end-stage heart failure. Circulation (1999) 1 0 0(19 Suppl.):11216–11223.
  • CORY CR, GRANGE RW, HOUSTON ME: Role of sarcoplasmic reticulum in loss of load-sensitive relaxation in pressure overload cardiac hypertrophy. Am. J. Physic)]. (1994) 2 6 6(1 Pt 2):H68–H78.
  • FRAZIER OH, BENEDICT CR, RADOVANCEVIC B et al.: Improved left ventricular function after chronic left ventricular unloading. Ann. Thorac. Surg. (1996) 62 (3) :675–681.
  • HEERDT PM, HOLMES JW, CAI B et al.: Chronic unloading by left ventricular assist device reverses contractile dysfunction and alters gene expression in end-stage heart failure. Circulation (2000) 102 (22):2713–2719.
  • LINDENMAYER GE, SCHWARTZ A: Nature of the transport adenosine triphosphatase digitalis complex. IV. Evidence that sodium-potassium competition modulates the rate of ouabain interaction with (Na±/K+ ) adenosine triphosphatase during enzyme catalysis. j Biol. Chem. (1973) 248 (4):1291–1300.
  • AFZAL N, PIERCE GN, ELIMBAN V, BEAMISH RE, DHALLANS: Influence of verapamil on some subcellular defects in diabetic cardiomyopathy. Am. J. Physiol. (1989) 256(4 Pt 1):E453–E458.
  • TEMSAH RM, DYCK C, NETTICADAN T et al: Effect of13-adrenocep tor blockers on sarcoplasmic reticular function and gene expression in the ischemic-rep er fused heart. J. Pharmacol. Exp. Ther. (2000) 293 (1):15–23.
  • •New aspects of protection by P-adrenergic receptor blockers.
  • TROTZ M, JELLISON EJ, HOSTETLER KY: Propranolol inhibition of the neutral phospholipases A of rat heart mitochondria, sarcoplasmic reticulum and cytosol. Biochem. Pharmacol (1987) 36(24):4251–4256.
  • YANAGISHITA T, KONNO N, GESHI E, KATAGIRI T: Alterations in phospholipids in acute ischemic myocardium. Jpn. Circ. J (1987) 51(1)41–50.
  • HOSTETLER KY, JELLISON EJ: Role of phospholipases inmyocardial ischemia: effect of cardioprotective agents on the phospholipases A of heart cytosol and sarcoplasmic reticulum in vitro. Mol. Cell Biochem. (1989) 88(1-2):77–82.
  • PANAGIA V, OU C, TAIRA Y, DAI J, DHALLA NS: Phospholipase D activity in subcellular membranes of rat ventricular myocardium. Biochim. Biophys. Acta (1991) 1064(2):242–250.
  • DAI J, MEIJ JT, DHALLA V, PANAGIA V: Involvement ofthiol groups in the impairment of cardiac sarcoplasmic reticular phospholipase D activity by oxidants.j LipidMediat. Cell Signal. (1995) 11 (2):107–118.
  • WILLIAMS SA, TAPPIA PS, YU CH et al: Subcellular altera-tions in cardiac phospholipase D activity in chronic diabetes. Prostaglandins Leukot. Essent. Fat t y Acids (1997) 57 (1):95–99.
  • HARTONG R, WANG N, KUROKAWA R et al.: Delineationof three different thyroid hormone-response elements in promoter of rat sarcoplasmic reticulum Ca2±ATPase gene. Demonstration that retinoid X receptor binds 5' to thyroid hormone receptor in response element 1.1 Biol. Chem. (1994) 269(17):13021–13029.
  • ROHRER DK, HARTONG R, DILLMANN WH: Influence ofthyroid hormone and retinoic acid on slow sarcoplasmic reticulum Ca2+ ATPase and myosin heavy chain alpha gene expression in cardiac myocytes. Delineation of cis-active DNA elements that confer responsiveness to thyroid hormone but not to retinoic acid. j Biol. Chem. (1991) 266(13):8638–8646.
  • MAHAFFEY KW, RAYA TE, PENNOCK GD, MORKIN E, GOLDMAN S: Left ventricular performance and remodeling in rabbits after myocardial infarction. Effects of a thyroid hormone analogue. Circulation (1995) 91 (3):794–801.
  • MORKIN E, PENNOCK GD, RAYA TE, BAHL JJ, GOLDMAN S: Studies on the use of thyroid hormone and a thyroid hormone analogue in the treatment of congestive heart failure. Ann. Thorac. Surg. (19 9 3) 5 6 (1 Suppl.):S54–S60.
  • KHOURY SF, HOIT BD, DAVE V et al.: Effects of thyroid hormone on left ventricular performance and regula-tion of contractile and Ca2+-cycling proteins in the baboon. Implications for the force-frequency and relaxation-frequency relationships. Circ. Res. (1996) 79 (4):727–735.
  • ZARAIN-HERZBERG A, RUPP H: Transcriptional modulators targeted at fuel metabolism of hypertro-phied heart. Am. J. Cardiol. (1999) 83 (12A):31H–37H.
  • ZARAIN-HERZBERG A, RUPP H, ELIMBAN V, DHALLA NS: Modification of sarcoplasmic reticulum gene expres-sion in pressure overload cardiac hypertrophy by etomoxir. FASEB J (1996) 10(10:1303–1309.
  • RUPP H, ELIMBAN V, DHALLA NS: Modification of myosin isozymes and SR Ca2±-pump ATPase of the diabetic rat heart by lipid-lowering interventions. Mol. Cell Biochem. (1994) 132(0:69–80.
  • RUPP H, ELIMBAN V, DHALLA NS: Modification of subcellular organelles in pressure-overloaded heart by etomoxir, a carnitine palmitoyltransferase I inhibitor. FASEB (1992) 6 (6):2349–2353.
  • YAMAGUCHI F, SANBE A, TAKEO S: Effects of long-term treatment with trandolapril on sarcoplasmic reticulum function of cardiac muscle in rats with chronic heart failure following myocardial infarction. Br. J. Pharmacol. (1998) 123 (2):326–334.
  • LIU X, SENTEX E, GOLFMAN L et al.: Modification of cardiac subcellular remodeling due to pressure overload by captopril and losartan. Clin. Exp. Hypertens. (1999) 21 (1-2):145–156.
  • SHAO Q, REN B, ZARAIN-HERZBERG A, GANGULY PK, DHALLA NS: Captopril treatment improves the sarcoplasmic reticular Ca2+ transport in heart failure due to myocardial infarction. j Mol. Cell Cardiol. (1999) 31 (9):1663–1672.
  • ANGER M, LAMBERT F, CHEMLA D et al.: Sarcoplasmic reticulum Ca2+ pumps in heart and diaphragm of cardiomyopathic hamster: effects of perindopril. Am. Physiol. (1995) 268(5 Pt 2):H1947–H1953.
  • FLESCH M, SCHIFFER F, ZOLK O et al.: Angiotensin receptor antagonism and angiotensin converting enzyme inhibition improve diastolic dysfunction and Ca2+-ATPase expression in the sarcoplasmic reticulum in hypertensive cardiomyopathy. j Hypertens. (1997) 15(9):1001–1009.
  • TAKEO S, NASA Y, TANONAKA K et al.: Role of cardiac renin-angiotensin system in sarcoplasmic reticulum function and gene expression in the isch emic-rep erfused heart. Mol. Cell Biochem. (2000) 212 (1-2):227–235.
  • YANAGISHITA T, TOMITA M, ITOH S et al.: Protective effect of captopril on ischemic myocardium. Jpn. Circ. J (1997) 61(2):161–169.
  • TAKEISHI Y, BHAGWAT A, BALL NA et al.: Effect of angiotensin-converting enzyme inhibition on protein kinase C and SRproteins in heart failure. Am. J Physiol. (1999) 276(1 Pt 2):H53–H62.
  • SPINALE FG, MUKHERJEE R, IANNINI JP et al.: Modulation of the renin-angiotensin pathway through enzyme inhibition and specific receptor blockade in pacing-induced heart failure: II. Effects on myocyte contrac-tile processes. Circulation (1997) 96 (7):2397–2406.
  • SAKAI S, MIYAUCHI T, YAMAGUCHI I: Long-term endothelin receptor antagonist administration improves alterations in expression of various cardiac genes in failing myocardium of rats with heart failure. Circulation (2000) 101 (24):2849–2853.
  • NEUMANN J, ESCHENHAGEN T, JONES LR et al.:Increased expression of cardiac phosphatases in patients with end-stage heart failure. j Mol. Cell Cardiol. (1997) 29(0:265–272.
  • REIMER KA, MURRY CE, YAMASAWA I, HILL ML, JENNINGS RB: Four brief periods of myocardial ischemia cause no cumulative ATP loss or necrosis. Am. J. Physiol. (1986) 251(6 Pt 2):H1306–15.
  • •First description of IP natural protection.
  • MURRY CE, JENNINGS RB, REIMER KA: Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation (1986) 74 (5) :1124–1136.
  • MARBER MS, WALKER DM, EVESON DJ, WALKER JM, YELLON DM: A single five minute period of rapid atrial pacing fails to limit infarct size in the in situ rabbit heart. Cardiovasc. Res. (1993) 27(4):597–601.
  • CAVE AC: Preconditioning induced protection againstpost-ischaemic contractile dysfunction: characteris-tics and mechanisms. J. Mol. Cell Cardiol. (1995) 27 (4):969–979.
  • KAWABATA K, OSADA M, NETTICADAN T, DHALLA NS:Beneficial effect of ischemic preconditioning on Ca2+ paradox in the rat heart. Life Sci. (1998) 63 (8):685–692.
  • OSADA M, NETTICADAN T, TAMURA K, DHALLA NS: Modification of ischemia-reperfusion-induced changes in cardiac sarcoplasmic reticulum by precon-ditioning. Am. J Physiol. (1998) 274(6 Pt 2) :H2025–H2034.
  • HAGAR JM, HALE SL, KLONER RA: Effect of precondi-tioning ischemia on reperfusion arrhythmias after coronary artery occlusion and reperfusion in the rat. Circ. Res. (1991) 68(0:61–68.
  • SHIKI K, HEARSE DJ: Preconditioning of ischemic myocardium: reperfusion-induced arrhythmias. Am. J. Physiol. (1987) 253(6 Pt 2):H1470–H1476.
  • TANI M, ASAKURA Y, HASEGAWA H et al.: Effect of preconditioning on ryanodine-sensitive Ca2+ release from sarcoplasmic reticulum of rat heart. Am. j Physiol (1996) 271(3 Pt 2):H876–H881.
  • TANI M, SUGANUMA Y, HASEGAWA H eta].: Changes in ischemic tolerance and effects of ischemic precondi-tioning in middle-aged rat hearts. Circulation (1997) 95 (11):2559–2566.
  • OSADA M, NETTICADAN T, KAWABATA K, TAMURA K, DHALLA NS: Ischemic preconditioning prevents I/R-induced alterations in SR calcium- calmodulin protein kinase II. Am]. Physiol. Heart Circ. Physiol. (2000) 278 (6):H1791–H1798.
  • KAWABATA KI, NETTICADAN T, OSADA M, TAMURA K, DHALLA NS: Mechanisms of ischemic preconditioning effects on Ca2+ paradox-induced changes in heart. Am. Physiol. Heart Circ. Physiol. (2000) 27 8 (3) :H1008–H1015.
  • MELDRUM DR, CLEVELAND JC, JR., MITCHELL MB et al.: Constructive priming of myocardium against ischemia-reperfusion injury. Shock (1996) 6 (4):238–242.
  • ZUCCHI R, YU G, GALBANI P et al.: Sulfhydryl redox state affects susceptibility to ischemia and sarcoplasmic reticulum Ca2+ release in rat heart. Implications for ischemic preconditioning. Circ. Res. (1998) 83(9):908–915.
  • MUSTERS RJ, VAN DER MEULEN ET, ZUIDWIJK M et al.: PKC-dependent preconditioning with norepineph-rine protects sarcoplasmic reticulum function in rat trabeculae following metabolic inhibition. j Mot. Cell Cardiol. (1999) 31(5):1083–1094.
  • NAGAI R, ZARAIN-HERZBERG A, BRANDL CJ et al.: Regulation of myocardial Ca2+-ATPase and phospho-lamban mRNA expression in response to pressure overload and thyroid hormone. Proc. Natl. Acad. Sci. USA (1989) 86(8):2966–2970.
  • ZARAIN-HERZBERG A, AFZAL N, ELIMBAN V, DHALLA NS: Decreased expression of cardiac sarcoplasmic reticulum Ca2+-pump ATPase in congestive heart failure due to myocardial infarction. Mot. Cell Biochem. (1996) 163–164:285–290.
  • LINCK B, BOKNIK P, ESCHENHAGEN T et al.: Messenger RNA expression and immunological quantification of phospholamban and SR-Ca2+-ATPase in failing and nonfailing human hearts. Cardiovasc. Res. (1996) 31 (4):625–632.
  • HE H, GIORDANO FJ, HILAL-DANDAN R et al.: Overex-pression of the rat sarcoplasmic reticulum Ca2+-ATPase gene in the heart of transgenic mice accelerates calcium transients and cardiac relaxation. Clin. Invest. (1997) 100 (2):380–389.
  • LOUKIANOV E, JI Y, GRUPP IL et al.: Enhanced myocar-dial contractility and increased Ca2+ transport function in transgenic hearts expressing the fast-twitch skeletal muscle sarcoplasmic reticulum Ca2+-ATPase. Circ. Res. (1998) 83 (9):889–897.
  • LUO W, GRUPP IL, HARRER J et al.: Targeted ablation of the phospholamban gene is associated with markedly enhanced myocardial contractility and loss of 13-agonist stimulation. Circ. Res. (1994) 75 (3):401–409.
  • KADAMBI VJ, PONNIAH S, HARRER JM et al.: Cardiac-specific overexpression of phospholamban alters calcium kinetics and resultant car diomyocyte mechanics in transgenic mice. J Clin. Invest. (1996) 97(2)533–539.
  • HADAR RJ, SCHMIDT U, KANG JX, MATSUI T, ROSENZ-WEIG A: Adenoviral gene transfer of phospholamban in isolated rat cardiomyocytes. Rescue effects by concomitant gene transfer of sarcoplasmic reticulum Ca2+-ATPase. Circ. Res. (1997) 81 (2) :145–153.
  • DEL M, HARDING SE, SCHMIDT U et al.: Restoration of contractile function in isolated cardiomyocytes from failing human hearts by gene transfer of SERCA2a. Circulation (1999) 10 0 (23) :2308–2311.
  • ••Gene therapy of failing human heart.
  • HASENFUSS G, MULIERI LA, LEAVITT BJ, ALPERT NR: Influence of isoproterenol on contractile protein function, excitation-contraction coupling, and energy turnover of isolated nonfailing human myocardium. j Mol. Cell. Cardiol. (1994) 26:1461–1469.

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