« Previous
Next »
Journal of Cardiac Failure
Volume 13, Issue 5
, Pages 401-414
, June 2007
Targeting Myocardial β-Adrenergic Receptor Signaling and Calcium Cycling for Heart Failure Gene Therapy
References
- American Heart Association. Heart disease and stroke statistics. Available from: www.americanheart.org/presenter.jhtml?presenter=2007. Accessed April 30, 2007.
- Trends in heart failure incidence and survival in a community-based population. JAMA. 2004;292:344–350
- . Epidemiology, pathophysiology, and etiology of congestive heart failure in older adults. J Am Geriatr Soc. 1997;45:968–974
- . Targeting calcium cycling proteins in heart failure through gene transfer. J Physiol. 2003;546:49–61
- . Viral-based myocardial gene therapy approaches to alter cardiac function. Annu Rev Physiol. 2004;66:49–75
- . Mechanisms of disease: β-adrenergic receptors-alterations in signal transduction and pharmacogenomics in heart failure. Nat Clin Pract Cardiovasc Med. 2005;2:475–483
- . The adrenergic pathway and heart failure. Recent Prog Horm Res. 2004;59:13–30
- . Calcium cycling in congestive heart failure. J Mol Cell Cardiol. 2002;34:951–969
- . Cardiac excitation-contraction coupling. Nature. 2002;415:198–205
- . Adrenergic and muscarinic receptors in the human heart. Pharmacol Rev. 1999;51:651–690
- . Model systems for the study of seven-transmembrane-segment receptors. Ann Rev Biochem. 1991;60:653–688
- . Regulation of cardiac ion channels by catecholamines, acetylcholine and second messenger systems. Prog Biophys Mol Biol. 1988;52:165–247
- . G protein βγ subunits. Annu Rev Pharmacol Toxicol. 1997;37:167–203
- . Seven-transmembrane-spanning receptors and heart function. Nature. 2002;415:206–212
- . β2-adrenergic receptor signaling complexes in cardiomyocyte caveolae/lipid rafts. J Mol Cell Cardiol. 2004;37:407–415
- Subtype-specific β-adrenoceptor signaling pathways in the heart and their potential clinical implications. Trends Pharmacol Sci. 2004;25:358–365
- . Opposing effects of β1- and β2-adrenergic receptors on cardiac myocytes apoptosis. Role of a pertussis toxin-sensitive G protein. Circulation. 1999;100:2210–2212
- . Dual modulation of cell survival and cell death by β2-adrenergic signaling in adult mouse cardiac myocytes. Proc Natl Acad Sci U S A. 2001;98:1607–1612
- . Turning off the signal: desensitization of β-adrenergic receptor function. FASEB J. 1990;4:2881–2889
- . Structure and mechanism of the G protein-coupled receptor kinases. J Biol Chem. 1993;268:23735–23738
- . Seven-transmembrane receptors. Nat Rev Mol Cell Biol. 2002;3:639–650
- . Endocytosis of G protein-coupled receptors: Roles of G protein-coupled receptor kinases and β-arrestin proteins. Prog Neurobiol. 2002;66:61–79
- . Regulation of G protein-coupled receptor kinases. Trends Cardiovasc Med. 2000;10:81–89
- . The binding site for the bg subunits of heterotrimeric G proteins on the β-adrenergic receptor kinase. J Biol Chem. 1993;268:8256–8260
- Cardiac function in mice overexpressing the β-adrenergic receptor kinase or a βARK inhibitor. Science. 1995;268:1350–1353
- . In vivo inhibition of elevated myocardial β-adrenergic receptor kinase in hybrid transgenic mice restores normal β-adrenergic signaling and function. Circulation. 1999;100:648–653
- . Preservation of myocardial β-adrenergic receptor signaling delays the development of heart failure after myocardial infarction. Proc Natl Acad Sci U S A. 2000;97:5428–5433
- Essential role of β-adrenergic receptor kinase 1 in cardiac development and function. Proc Natl Acad Sci U S A. 1996;93:12974–12979
- Regulation of myocardial contractile function by the level of β-adrenergic receptor kinase-1 in gene targeted mice. J Biol Chem. 1998;273:18180–18184
- Decreased catecholamine sensitivity and β-adrenergic receptor density in failing human hearts. New Engl J Med. 1982;307:205–211
- Reduced β1 receptor messenger RNA abundance in the failing human heart. J Clin Invest. 1993;92:2737–2745
- . Altered expression of β-adrenergic receptor kinase and β1-adrenergic receptors in the failing human heart. Circulation. 1993;87:454–463
- β1-adrenergic receptor polymorphisms confer differential function and predisposition to heart failure. Nat Med. 2003;9:1300–1305
- The Ile164 β2-adrenergic receptor polymorphism adversely affects the outcome of congestive heart failure. J Clin Invest. 1998;102:1534–1539
- . The β-adrenergic receptor kinase in heart failure. J Mol Cell Cardiol. 2003;35:1167–1174
- . Characterization of lymphocyte β2-adrenoceptor signaling in patients with left ventricular volume overload disease. Clin Exp Pharmacol Physiol. 2002;29:181–188
- . Differential functional expression of human myocardial G protein receptor kinases in left ventricular cardiac diseases. Eur J Pharmacol. 2004;489:167–177
- . Expression of GRK2 is increased in the left ventricles of cardiomyopathic hamsters. Basic Res Cardiol. 2001;96:364–368
- . Enhanced contractility and decreased β-adrenergic receptor kinase-1 in mice lacking endogenous norepinephrine and epinephrine. Circulation. 1999;99:2702–2707
- . The myocardial β-adrenergic system in spontaneously hypertensive herat failure (SHHF) rats. Hypertension. 1999;33:402–407
- Expression of a β-adrenergic receptor kinase 1 inhibitor prevents the development of myocardial failure in gene-targeted mice. Proc Natl Acad Sci U S A. 1998;95:7000–7005
- . Myocyte redistribution of GRK2 and GRK5 in hypertensive, heart-failure-prone rats. Hypertension. 2002;39:1058–1063
- . Myocardial distribution and regulation of GRK and β-arrestin isoforms in congestive heart failure in rats. Am J Physiol Heart Circ Physiol. 2001;281:H2490–H2499
- . Adenylyl cyclase and G protein receptor kinase expression during development of heart failure. Am J Physiol Heart Circ Physiol. 1997;273:H707–H717
- . Activation of β-adrenergic receptor kinase during myocardial ischemia. Circ Res. 1996;79:455–460
- . Mechanism of β-adrenergic receptor desensitization in cardiac hypertrophy is increased β-adrenergic receptor kinase. J Biol Chem. 1997;272:17223–17229
- . G-protein-coupled receptor kinase activity is increased in hypertension. J Clin Invest. 1997;99:2087–2093
- Regulation of myocardial βARK1 expression in catecholamine-induced cardiac hypertrophy in transgenic mice overexpressing α1B-adrenergic receptors. J Am Coll Cardiol. 2001;38:534–540
- . Neurohormonal activation in patients with acute myocardial infarction or chronic congestive heart failure. 1. Blood Press; 1995;1–45
- . Increased cardiac adrenergic drive precedes generalized sympathetic activation in human heart failure. Circulation. 1997;95:169–175
- . β-adrenergic receptor kinase-1 levels in catecholamine-induced myocardial hypertrophy: regulation by β- but not α1-adrenergic stimulation. Hypertension. 1999;33:396–401
- . Reciprocal in vivo regulation of myocardial G protein-coupled receptor expression by β-adrenergic receptor stimulation and blockade. Circulation. 1998;98:1783–1789
- Plasma norepinephrine as a guide to prognosis in patients with chronic congestive heart failure. N Engl J Med. 1984;311:819–823
- . The development of positive inotropic agents for chronic heart failure: how have we gone astray?. J Am Coll Cardiol. 1993;22:119A–126A
- Randomized evaluation of mechanical assistance for the treatment of congestive heart failure (REMATCH) study group. N Engl J Med. 2001;345:1435–1443
- . Myocyte recovery after mechanical circulatory support in humans with end-stage heart failure. Circulation. 1998;97:2316–2322
- . Mechanical unloading restores β-adrenergic responsiveness and reverses receptor downregulation in the failing human heart. Circulation. 2001;104:881–886
- Lymphocyte levels of GRK2 (βARK1) mirror changes in the LVAD-supported failing human heart: lower GRK2 associated with improved β-adrenergic signaling after mechanical unloading. J Card Fail. 2006;12:360–368
- Elevated myocardial and lymphocyte GRK2 expression in human heart failure. Eur Heart J. 2005;26:1752–1758
- . Tissue-specific regulation of the α-myosin heavy chain gene promoter in transgenic mice. J Biol Chem. 1991;266:24613–24620
- Myocardial-directed overexpression of the human β1-adrenergic receptor in transgenic mice. J Mol Cell Cardiol. 2000;32:817–830
- . Progressive hypertrophy and heart failure in β1-adrenergic receptor transgenic mice. Proc Natl Acad Sci U S A. 1999;96:7059–7064
- Enhanced myocardial function in transgenic mice overexpressing the β2-adrenergic receptor. Science. 1994;264:582–586
- Augmentation of cardiac contractility mediated by the human β3-adrenergic receptor overexpressed in the hearts of transgenic mice. Circulation. 2001;104:2485–2491
- . Myocardial overexpression of GRK3 in transgenic mice: evidence for in vivo selectivity of GRKs. Am J Physiol Heart Circ Physiol. 1998;275:H1298–H1306
- . Receptor-specific in vivo desensitization by the G protein-coupled receptor kinase-5 in transgenic mice. Proc Natl Acad Sci U S A. 1996;93:9954–9959
- . Genetic manipulation of myocardial β-adrenergic receptor activation and desensitization. J Mol Cell Cardiol. 2004;37:11–21
- Early and delayed consequences of β2-adrenergic receptor overexpression in mouse hearts: critical role for expression level. Circulation. 2000;101:1707–1714
- Coupling of β2-adrenoceptor to Gi proteins and its physiological relevance in murine cardiac myocytes. Circ Res. 1999;84:43–52
- The effect of Gi-protein inactivation on basal, and β1- and β2AR-stimulated contraction of myocytes from transgenic mice overexpressing the β2-adrenoceptor. Br J Pharmacol. 2000;131:594–600
- . Protein kinase C regulates functional coupling of β1-adrenergic receptors to Gi/o-mediated responses in cardiac myocytes. FASEB J. 2004;18:367–369
- Restoration of β-adrenergic signaling in failing cardiac ventricular myocytes via adenoviral-mediated gene transfer. Proc Natl Acad Sci U S A. 1997;94:12100–12105
- . Potentiation of β-adrenergic signaling by adenoviral-mediated gene transfer in adult rabbit ventricular myocytes. J Clin Invest. 1997;99:288–296
- Enhancement of cardiac function after adenoviral-mediated in vivo intracoronary β2-adrenergic receptor gene delivery. J Clin Invest. 1999;104:21–29
- Intracoronary adenovirus-mediated delivery and overexpression of the β2-adrenergic receptor in the heart: prospects for molecular ventricular assistance. Circulation. 2000;101:408–414
- In vivo transfer of a β2-adrenergic receptor gene into the pressure-overloaded rat heart enhances cardiac response to β-adrenergic agonist. Circulation. 1998;98:II262–II267
- Adenovirus-mediated gene transfer of the β2-adrenergic receptor to donor hearts enhances cardiac function. Gene Ther. 1999;6:1298–1304
- . Myocardial gene transfer and overexpression of β2-adrenergic receptors potentiates the functional recovery of unloaded failing hearts. Circulation. 2002;106:124–129
- . Bridge to recovery with the use of left ventricular assist device and clenbuterol. Ann Thorac Surg. 2003;75:S36–S41
- . Left ventricular assist device and drug therapy for the reversal of heart failure. N Engl J Med. 2006;355:1873–1884
- . Cardiac βARK1 inhibition prolongs survival and augments β blocker therapy in a mouse model of severe heart failure. Proc Natl Acad Sci U S A. 2001;98:5809–5814
- . Defective β-adrenergic receptor signaling precedes the development of dilated cardiomyopathy in transgenic mice with calsequestrin overexpression. J Biol Chem. 1999;274:22251–22256
- Alterations in cardiac adrenergic signaling and calcium cycling differentially affect the progression of cardiomyopathy. J Clin Invest. 2001;107:967–974
- . Expression of a β-adrenergic receptor kinase inhibitor reverses dysfunction in failing cardiomyocytes. Mol Ther. 2002;5:74–79
- Targeted β-adrenergic receptor kinase (βARK1) inhibition by gene transfer in failing human hearts. Circulation. 2004;109:1590–1593
- In vivo ventricular gene delivery of a β-adrenergic receptor kinase inhibitor to the failing heart reverses cardiac dysfunction. Circulation. 2001;103:1311–1316
- Catheter-based intracoronary myocardial adenoviral gene delivery: importance of intraluminal seal and infusion flow-rate. Mol Ther. 2003;8:306–313
- Catheter-mediated subselective intracoronary gene delivery to the rabbit heart: introduction of a novel method. J Gene Med. 2005;7:595–603
- . Right ventricular gene therapy with a β-adrenergic receptor kinase inhibitor improves survival after pulmonary artery banding. Ann Thor Surg. 2001;72:1657–1661
- Right ventricular targeted gene transfer of a β-adrenergic receptor kinase inhibitor improves ventricular performance after pulmonary artery banding. J Thorac Cardiovasc Surg. 2004;127:787–793
- . Ventricular dysfunction after cardioplegic arrest is improved after myocardial gene transfer of a β-adrenergic receptor kinase inhibitor. Circulation. 2001;104:2069–2074
- . Acute ischemic cardiac dysfunction is attenuated via gene transfer of a peptide inhibitor of the β-adrenergic receptor kinase (βARK1). J Gene Med. 2005;7:1172–1177
- Adverse effects of chronic endogenous sympathetic drive induced by cardiac Gsα overexpression. Circ Res. 1996;78:517–524
- Apoptosis of cardiac myocytes in Gsα transgenic mice. Circ Res. 1999;84:34–42
- Adenylyl cyclase increases responsiveness to catecholamine stimulation in transgenic mice. Circulation. 1999;99:1618–1622
- Transgenic Gαq overexpression induces cardiac contractile failure in mice. Proc Natl Acad Sci U S A. 1997;94:8121–8126
- Cardiac-directed adenylyl cyclase expression improves heart function in murine cardiomyopathy. Circulation. 1999;99:3099–3102
- Adenylyl cyclase increases survival in cardiomyopathy. Circulation. 2002;105:1989–1994
- Intracoronary delivery of adenovirus encoding adenylyl cyclase VI increases left ventricular function and cAMP-generating capacity. Circulation. 2000;102:2396–2401
- Intracoronary adenovirus encoding adenylyl cyclase VI increases left ventricular function in heart failure. Circulation. 2004;110:330–336
- Interactions between phospholamban and β-adrenergic drive may lead to cardiomyopathy and early mortality. Circulation. 2001;103:889–896
- . Geneticaly engineered models with alterations in cardiac membrane calcium-handling proteins. Annu Rev Physiol. 2000;62:321–351
- . Abnormalities of calcium cycling in the hypertrophied and failing heart. J Mol Cell Cardiol. 2000;32:1595–1607
- PKA phosphorylation dissociates FKBP126 from the calcium release channel (ryanodine receptor): effective regulation in failing hearts. Cell. 2000;101:365–376
- . Ca2+/calmodulin-dependent protein kinase II phosphorylation regulates the cardiac ryanodine receptor. Circ Res. 2004;94:e61–e70
- . Nitric oxide signaling in the cardiovascular system: implications for heart failure. Curr Opin Cardiol. 2006;21:221–228
- . Activation of the cardiac calcium release channel (ryanodine receptor) by poly-S-nitrosylation. Science. 1998;279:234–237
- . Free radical-induced protein modification and inhibition of Ca2+-ATPase of cardiac sarcoplasmic reticulum. Mol Cell Biochem. 2003;248:41–47
- . Dynamic regulation of sodium/calcium exchange function in human heart failure. Circulation. 2003;108:2224–2229
- . Rate of diastolic Ca2+ release from the sarcoplasmic reticulum of intact rabbit and rat ventricular myocytes. Biophys J. 1995;68:2015–2022
- . Targeting Ca2+ cycling proteins and the action potential in heart failure by gene transfer. Basic Res Cardiol. 2002;97:I136–I145
- . Na/Ca exchange in heart failure: contractile dysfunction and arrhythmogenesis. Ann NY Acad Sci. 2002;976:454–465
- . Upregulated Na/Ca exchange is involved in both contractile dysfunction and arrhythmogenesis in heart failure. Basic Res Cardiol. 2002;97:I36–I42
- . Sarcoplasmic reticulum Ca-ATPase-phospholamban interactions and dilated cardiomyopathy. Biochem Biophys Res Commun. 2004;322:1214–1222
- . Functional roles of S100 proteins, calcium-binding proteins of the EF-hand type. Biochim Biophys Acta. 1999;1450:191–231
- . Ultrastructual distribution of the S100A1 Ca2+-binding protein in the human heart. Physiol Res. 2001;50:567–574
- Most P, Remppis A, Pleger ST, Katus HA, Koch WJ. S100A1: a novel inotropic regulator of cardiac performance. Transition from molecular physiology to pathophysiological relevance. Am J Physiol Regu Integr Comp Physiol 2007 Apr 25 [Epub ahead of print] doi:10.1152/ajpregu.00075.2007.
- Altered expression of the Ca2+-binding protein S100A1 in human cardiomyopathy. Biochim Biophys Acta. 1996;1313:253–257
- Distinct subcellular location of the Ca2+-binding protein S100A1 differentially modulates Ca2+-cycling in ventricular rat cardiomyocytes. J Cell Sci. 2005;118:421–431
- Genetic modification of engineered heart tissue (EHT): S100A1 gene transfer strengthens EHT. J Gene Med. 2004;6:387–394
- The small EF-hand Ca2+ binding protein S100A1 increases contractility and Ca2+ cycling in rat cardiac myocytes. Basic Res Cardiol. 2002;97:I56–I62
- S100A1: A novel regulator of myocardial contractility. Proc Natl Acad Sci U S A. 2001;98:13889–13894
- . S100A1 increases the gain of excitation-contraction coupling in isolated rabbit ventricular cardiomyocytes. J Mol Cell Cardiol. 2005;39:900–910
- Cardiac adenoviral S100A1 gene delivery rescues failing myocardium. J Clin Invest. 2004;114:1550–1563
- S100A1 decreases calcium spark frequency and alters their characteristics in permeabilized adult ventricular cardiomyocytes. Cell Calcium. 2007;41:135–143
- S-100a. protein in serum during acute myocardial infarction. Clin Chem. 1990;36:639–641
- . S100A1 is a novel molecular chaperone and a member of the Hsp70/Hsp90 multichaperone complex. J Biol Chem. 2004;279:4221–4233
- Extracellular S100A1 protein inhibits apoptosis in ventricular cardiomyocytes via activation of the extracellular signal-regulated protein kinase 1/2 (ERK1/2). J Biol Chem. 2003;278:48404–48412
- Transgenic overexpression of the Ca2+ binding protein S100A1 in the heart leads to increased in vivo myocardial contractile performance. J Biol Chem. 2003;278:33809–33817
- Cardiac S100A1 protein levels determine contractile performance and propensity towards heart failure after myocardial infarction. Circulation. 2006;114:1258–1268
- . Redox modifications of the C-terminal cysteine residue cause structural changes in S100A1 and S100B proteins. Biochim Biophys Acta. 2004;1742:191–201
- S100A1 gene therapy preserves in vivo cardiac function after myocardial infarction. Mol Ther. 2005;12:1120–1129
- . The myocardial protein S100A1 plays a role in the maintenance of normal gene expression in the adult heart. Mol Cell Biochem. 2003;242:27–33
- Impaired cardiac contractility response to hemodynamic stress in S100A1-deficient mice. Mol Cell Biochem. 2002;22:2821–2829
- Boerries M, Most P, Gledhill JR, Walker JE, Katus HA, Koch WJ, et al. The Ca2+-dependent interaction of S100A1 with the F1-ATPase leads to an increased ATP content in cardiomyocytes. Mol Cell Biol 2007; Apr 16 [Epub ahead of print] doi:10.1128/MCB.02045-06.
- Stable myocardial-specific AAV6-S100A1 gene therapy results in chronic functional heart failure rescue. Circulation. 2007;115:2506–2515
The work of S.T.P. is supported by an American Heart Association postdoctoral fellow award. M.B. is supported by an American Heart Association postdoctoral fellow award and a Fonds de la Recherche en Santé du Québec postdoctoral scholarship. P.M. is supported by the Deutsche Forschungsgemeinschaft (MO 1066/1-1) and the Bundesministerium fuer Bildung und Forschung (01GU0527). W.J.K. is a Fellow of the American Heart Association (FAHA) and is supported by National Institute of Health R01 grants HL61690, HL56205 and P01-HL075443 (Project 2).S.T.P. and M.B. contributed equally to this article.
PII: S1071-9164(07)00004-8
doi: 10.1016/j.cardfail.2007.01.003
© 2007 Elsevier Inc. All rights reserved.
« Previous
Next »
Journal of Cardiac Failure
Volume 13, Issue 5
, Pages 401-414
, June 2007
