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Science 24 April 1998:
Vol. 280. no. 5363, pp. 574 - 577
DOI: 10.1126/science.280.5363.574
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Reports

Targeting the Receptor-Gq Interface to Inhibit in Vivo Pressure Overload Myocardial Hypertrophy

Shahab A. Akhter, Louis M. Luttrell, Howard A. Rockman, Guido Iaccarino, Robert J. Lefkowitz, Walter J. Koch *

Hormones and neurotransmitters may mediate common responses through receptors that couple to the same class of heterotrimeric guanine nucleotide-binding (G) protein. For example, several receptors that couple to Gq class proteins can induce cardiomyocyte hypertrophy. Class-specific inhibition of Gq-mediated signaling was produced in the hearts of transgenic mice by targeted expression of a carboxyl-terminal peptide of the alpha  subunit Galpha q. When pressure overload was surgically induced, the transgenic mice developed significantly less ventricular hypertrophy than control animals. The data demonstrate the role of myocardial Gq in the initiation of myocardial hypertrophy and indicate a possible strategy for preventing pathophysiological signaling by simultaneously blocking multiple receptors coupled to Gq.

S. A. Akhter and W. J. Koch, Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA.
L. M. Luttrell, Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
H. A. Rockman, Department of Medicine (Cardiology), University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
G. Iaccarino and R. J. Lefkowitz, Howard Hughes Medical Institute, Departments of Medicine and Biochemistry, Duke University Medical Center, Durham, NC 27710, USA.
*   To whom correspondence should be addressed. E-mail: koch0002{at}mc.duke.edu

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MEKK1 is essential for cardiac hypertrophy and dysfunction induced by Gq.
T. Minamino, T. Yujiri, N. Terada, G. E. Taffet, L. H. Michael, G. L. Johnson, and M. D. Schneider (2002)
PNAS 99, 3866-3871
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Adenoviral-Directed Expression of the Type 1A Angiotensin Receptor Promotes Cardiomyocyte Hypertrophy via Transactivation of the Epidermal Growth Factor Receptor.
W. G. Thomas, Y. Brandenburger, D. J. Autelitano, T. Pham, H. Qian, and R. D. Hannan (2002)
Circ. Res. 90, 135-142
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G{alpha} COOH-Terminal Minigene Vectors Dissect Heterotrimeric G Protein Signaling.
A. Gilchrist, A. Li, and H. E Hamm (2002)
Sci. STKE 2002, pl1
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Flt-1-mediated Down-regulation of Endothelial Cell Proliferation through Pertussis Toxin-sensitive G Proteins, beta gamma Subunits, Small GTPase CDC42, and Partly by Rac-1.
H. Zeng, D. Zhao, and D. Mukhopadhyay (2002)
J. Biol. Chem. 277, 4003-4009
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Apoptosis Signal-Regulating Kinase/Nuclear Factor-{kappa}B: A Novel Signaling Pathway Regulates Cardiomyocyte Hypertrophy.
T. Force, S. Haq, H. Kilter, and A. Michael (2002)
Circulation 105, 402-404
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Involvement of G Proteins in Vascular Permeability Factor/ Vascular Endothelial Growth Factor Signaling.
D. MUKHOPADHYAY and H. ZENG (2002)
Cold Spring Harb Symp Quant Biol 67, 275-284
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G-Protein-coupled Receptor Function in Heart Failure.
S.V. NAGA PRASAD, J. NIENABER, and H.A. ROCKMAN (2002)
Cold Spring Harb Symp Quant Biol 67, 439-444
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Still Stressed Out but Doing Fine: Normalization of Wall Stress Is Superfluous to Maintaining Cardiac Function in Chronic Pressure Overload.
M. Sano and M. D. Schneider (2002)
Circulation 105, 8-10
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Genetic Alterations That Inhibit In Vivo Pressure-Overload Hypertrophy Prevent Cardiac Dysfunction Despite Increased Wall Stress.
G. Esposito, A. Rapacciuolo, S. V. Naga Prasad, H. Takaoka, S. A. Thomas, W. J. Koch, and H. A. Rockman (2002)
Circulation 105, 85-92
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Activation of Protein Kinase D by Signaling through Rho and the alpha Subunit of the Heterotrimeric G Protein G13.
J. Yuan, L. W. Slice, and E. Rozengurt (2001)
J. Biol. Chem. 276, 38619-38627
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Transgenic Studies of Cardiac Adrenergic Receptor Regulation.
A. D. Eckhart and W. J. Koch (2001)
J. Pharmacol. Exp. Ther. 299, 1-5
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Important role of endogenous norepinephrine and epinephrine in the development of in vivo pressure-overload cardiac hypertrophy.
A. Rapacciuolo, G. Esposito, K. Caron, L. Mao, S. A. Thomas, and H. A. Rockman (2001)
J. Am. Coll. Cardiol. 38, 876-882
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Regulation of myocardial {beta}ARK1 expression in catecholamine-induced cardiac hypertrophy in transgenic mice overexpressing {alpha}1B-adrenergic receptors.
G. Iaccarino, J. R. Keys, A. Rapacciuolo, K. F. Shotwell, R. J. Lefkowitz, H. A. Rockman, and W. J. Koch (2001)
J. Am. Coll. Cardiol. 38, 534-540
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Progress in Understanding the Etiology of Thyroid Autonomy.
K. Krohn and R. Paschke (2001)
J. Clin. Endocrinol. Metab. 86, 3336-3345
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Genetic Analysis of the Drosophila Gs{{alpha}} Gene.
W. J. Wolfgang, A. Hoskote, I. J. H. Roberts, S. Jackson, and M. Forte (2001)
Genetics 158, 1189-1201
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Sympathoadrenergic mechanisms in functional regulation and development of cardiac hypertrophy and failure: findings from genetically engineered mice.
X.-J. Du (2001)
Cardiovasc Res 50, 443-453
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To Cre or Not To Cre : The Next Generation of Mouse Models of Human Cardiac Diseases.
K. R. Chien (2001)
Circ. Res. 88, 546-549
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Cardiac Overexpression of a Gq Inhibitor Blocks Induction of Extracellular Signal-Regulated Kinase and c-Jun NH2-Terminal Kinase Activity in In Vivo Pressure Overload.
G. Esposito, S. V. N. Prasad, A. Rapacciuolo, L. Mao, W. J. Koch, and H. A. Rockman (2001)
Circulation 103, 1453-1458
   Abstract »    Full Text »    PDF »
G Proteins and Heart Failure : Is G{alpha}q a Novel Target for Heart Failure?.
G. Z. Feuerstein and D. Rozanski (2000)
Circ. Res. 87, 1085-1086
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Physiological Induction of a {beta}-Adrenergic Receptor Kinase Inhibitor Transgene Preserves {beta}-Adrenergic Responsiveness in Pressure-Overload Cardiac Hypertrophy.
B. S. Manning, K. Shotwell, L. Mao, H. A. Rockman, and W. J. Koch (2000)
Circulation 102, 2751-2757
   Abstract »    Full Text »    PDF »


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