Abstract
Cardiac overload initiates a process, which aims to maintain and adapt cardiovascular system to altered hemodynamics. In adults, myocardial mass increases mainly due to enlargement of individual myocytes (for reviews, see refs. 1,2). Cardiac pressure overload in conditions such as aortic stenosis or hypertension, results in parallel addition of sarcomeres and increases width of myocytes, which in turn, augment left ventricular wall thickness.2 However, when mechanical and neurohumoral stress are sustained, the adaptive mechanisms eventually fail and further myocardial remodelling leads to ventricular dilation and impairment of cardiac contractile function. Cardiac output reduces until being inadequate to maintain efficient blood circulation of the whole organism and the syndrome of congestive heart failure occurs.2,3 At the cellular level, the cardiac growth and failure is due to a complex pattern of signaling mechanisms and molecules. In 1980s, identification of genes associated with cardiac hypertrophy were accompanied by the discovery of natriuretic peptides in the heart.4,5 Since then, this has been followed by characterization of regulatory mechanisms in natriuretic peptide secretion and synthesis and further insight of the signaling mechanisms and of the development of cardiac hypertrophy has been achieved.
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References
Swynghedauw B. Molecular mechanisms of myocardial remodeling. Physiol Rev 1999; 79:215–262.
Lorell BH, Carabello BA. Left ventricular hypertrophy: Pathogenesis, detection, and prognosis. Circulation 2000; 102:470–479.
Hunter JJ, Chien KR. Signaling pathways for cardiac hypertrophy and failure. N Engl J Med 1999; 341:1276–1283.
de Bold AJ, Borenstein HB, Veress AT et al. A rapid and potent natriuretic response to intravenous injection of atrial myocardial extract in rats. Life Sci 1981; 28:89–94.
Ruskoaho H. Atrial natriuretic peptide: Synthesis, release, and metabolism. Pharmacol Rev 1992; 44:479–602.
Nakayama K, Ohkubo H, Hirose T et al. mRNA sequence for human cardiodilatin-atrial natriuretic factor precursor and regulation of precursor mRNA in rat atria. Nature 1984; 310:699–701.
Greenberg BD, Bencen GH, Seilhamer JJ et al. Nucleotide sequence of the gene encoding human atrial natriuretic factor precursor. Nature 1984; 312:656–658.
Yamanaka M, Greenberg B, Johnson L et al. Cloning and sequence analysis of the cDNA for the rat atrial natriuretic factor precursor. Nature 1984; 309:719–722.
Sudoh T, Kangawa K, Minamino N et al. A new natriuretic peptide in porcine brain. Nature 1988; 332:78–81.
Sudoh T, Minamino N, Kangawa K et al. C-type natriuretic peptide (CNP): A new member of natriuretic peptide family identified in porcine brain. Biochem Biophys Res Commun 1990; 168:863–870.
Ogawa Y, Nakao K, Mukoyama M et al. Natriuretic peptides as cardiac hormones in normotensive and spontaneously hypertensive rats. The ventricle is a major site of synthesis and secretion of brain natriuretic peptide. Circ Res 1991; 69:491–500.
Gerbes AL, Dagnino L, Nguyen T et al. Transcription of brain natriuretic peptide and atrial natriuretic peptide genes in human tissues. J Clin Endocrinol Metab 1994; 78:1307–1311.
Komatsu Y, Nakao K, Suga S et al. C-type natriuretic peptide (CNP) in rats and humans. Endocrinology 1991; 129:1104–1106.
Chun TH, Itoh H, Ogawa Y et al. Shear stress augments expression of C-type natriuretic peptide and adrenomedullin. Hypertension 1997; 29:1296–1302.
Schweitz H, Vigne P, Moinier D et al. A new member of the natriuretic peptide family is present in the venom of the green mamba (Dendroaspis angusticeps). J Biol Chem 1992; 267:13928–13932.
Majalahti-Palviainen T, Hirvinen M, Tervonen V et al. Gene structure of a new cardiac peptide hormone: A model for heart-specific gene expression. Endocrinology 2000; 141:731–740.
Nakao K, Ogawa Y, Suga S et al. Molecular biology and biochemistry of the natriuretic peptide system. II: Natriuretic peptide receptors. J Hypertens 1992b; 10:1111–1114.
Potter LR, Hunter T. Guanylyl cyclase-linked natriuretic peptide receptors: Structure and regulation. J Biol Chem 2001; 276:6057–6060.
Levin ER, Gardner DG, Samson WK. Natriuretic peptides. N Engl J Med 1998; 339:321–328.
Yandle TG. Biochemistry of natriuretic peptides. J Intern Med 1994; 235:561–576.
Yan W, Wu F, Morser J et al. Corin, a transmembrane cardiac serine protease, acts as a pro-atrial natriuretic peptide-converting enzyme. Proc Natl Acad Sci USA 2000; 97:8525–8529.
Wu F, Yan W, Pan J et al. Processing of pro-atrial natriuretic peptide by corin in cardiac myocytes. J Biol Chem 2002; 277:16900–16905.
Nakao K, Ogawa Y, Suga S et al. Molecular biology and biochemistry of the natriuretic peptide system. I: Natriuretic peptides. J Hypertens 1992a; 10:907–912.
Mäntymaa P, Vuolteenaho O, Marttila M et al. Atrial stretch induces rapid increase in brain natriuretic peptide but not in atrial natriuretic peptide gene expression in vitro. Endocrinology 1993; 133:1470–1473.
Wei CM, Heublein DM, Perrella MA et al. Natriuretic peptide system in human heart failure. Circulation 1993; 88:1004–1009.
Sadoshima J, Izumo S. Mechanical stretch rapidly activates multiple signal transduction pathways in cardiac myocytes: Potential involvement of an autocrine/paracrine mechanism. EMBO J 1993; 12:1681–1692.
Komuro I, Kaida T, Shibazaki Y et al. Stretching cardiac myocytes stimulates protooncogene expression. J Biol Chem 1990; 265:3595–3598.
Yamazaki T, Komuro I, Yazaki Y. Molecular mechanism of cardiac cellular hypertrophy by mechanical stress. J Mol Cell Cardiol 1995c; 27:133–140.
Tokola H, Hautala N, Marttila M et al. Mechanical load-induced alterations in B-type natriuretic peptide gene expression. Can J Physiol Pharmacol 2001; 79:646–653.
Izumo S, Lompre AM, Matsuoka R et al. Myosin heavy chain messenger RNA and protein isoform transitions during cardiac hypertrophy. Interaction between hemodynamic and thyroid hormone-induced signals. J Clin Invest 1987; 79:970–977.
Nakao K, Minobe W, Roden R et al. Myosin heavy chain gene expression in human heart failure. J Clin Invest 1997; 100:2362–2370.
Magga J, Marttila M, Mäntymaa P et al. Brain natriuretic peptide in plasma, atria, and ventricles of vasopre. Endocrinology 1994; 134:2505–2515.
Magga J, Vuolteenaho O, Marttila M et al. Endothelin-1 is involved in stretch-induced early activation of B-type natriuretic peptide gene expression in atrial but not in ventricular myocytes: Acute effects of mixed ET(A)/ET(B) and AT1 receptor antagonists in vivo and in vitro. Circulation 1997a; 96:3053–3062.
Bruneau BG, Piazza LA, de Bold AJ. BNP gene expression is specifically modulated by stretch and ET-1 in a new model of isolated rat atria. Am J Physiol 1997; 273:H2678–H2686.
Magga J, Vuolteenaho O, Tokola H et al. Involvement of transcriptional and posttranscriptional mechanisms in cardiac overload-induced increase of B-type natriuretic peptide gene expression. Circ Res 1997b; 81:694–702.
Liang F, Wu J, Garami M et al. Mechanical strain increases expression of the brain natriuretic peptide gene in rat cardiac myocytes. J Biol Chem 1997; 272:28050–28056.
Adachi S, Ito H, Ohta Y et al. Distribution of mRNAs for natriuretic peptides in RV hypertrophy after pulmonary arterial banding. Am J Physiol 1995; 268:H162–H169.
Sadoshima J, Xu Y, Slayter HS et al. Autocrine release of angiotensin II mediates stretch-induced hypertrophy of cardiac myocytes in vitro. Cell 1993; 75:977–984.
Liang F, Gardner DG. Autocrine/paracrine determinants of strain-activated brain natriuretic peptide gene expression in cultured cardiac myocytes. J Biol Chem 1998; 273:14612–14619.
Kaye D, Pimental D, Prasad S et al. Role of transiently altered sarcolemmal membrane permeability and basic fibroblast growth factor release in the hypertrophic response of adult rat ventricular myocytes to increased mechanical activity in vitro. J Clin Invest 1996; 97:281–291.
Yamazaki T, Komuro I, Kudoh S et al. Endothelin-1 is involved in mechanical stress-induced cardiomyocyte hypertrophy. J Biol Chem 1996; 271:3221–3228.
Yamazaki T, Komuro I, Kudoh S et al. Angiotensin II partly mediates mechanical stress-induced cardiac hypertrophy. Circ Res 1995a; 77:258–265.
Ito H, Hirata Y, Adachi S et al. Endothelin-1 is an autocrine/paracrine factor in the mechanism of angiotensin II-induced hypertrophy in cultured rat cardiomyocytes. J Clin Invest 1993; 92:398–403.
Harada M, Itoh H, Nakagawa O et al. Significance of ventricular myocytes and nonmyocytes interaction during cardiocyte hypertrophy: Evidence for endothelin-1 as a paracrine hypertrophic factor from cardiac nonmyocytes. Circulation 1997; 96:3737–3744.
Harada K, Komuro I, Shiojima I et al. Pressure overload induces cardiac hypertrophy in angiotensin II type 1A receptor knockout mice. Circulation 1998; 97:1952–1959.
Nyui N, Tamura K, Mizuno K et al. Stretch-induced MAP kinase activation in cardiomyocytes of angiotensinogen-deficient mice. Biochem Biophys Res Commun 1997; 235:36–41.
Kudoh S, Komuro I, Hiroi Y et al. Mechanical stretch induces hypertrophic responses in cardiac myocytes of angiotensin II type la receptor knockout mice. J Biol Chem 1998; 273:24037–24043.
Porter JG, Arfsten A, Palisi T et al. Cloning of a cDNA encoding porcine brain natriuretic pep-tide. J Biol Chem 1989; 264:6689–6692.
Shaw G, Kamen R. A conserved AU sequence from the 3′ untranslated region of GM-CSF mRNA mediates selective mRNA degradation. Cell 1986; 46:659–667.
Hanford DS, Glembotski CC. Stabilization of the B-type natriuretic peptide mRNA in cardiac myocytes by alpha-adrenergic receptor activation: Potential roles for protein kinase C and mitogen-activated protein kinase. Mol Endocrinol 1996; 10:1719–1727.
Suo M, Hautala N, Földes G et al. Posttranscriptional control of BNP gene expression in angiotensin II-induced hypertension. Hypertension 2002; 39:803–808.
Tavi P, Laine M, Weckström M et al. Cardiac mechanotransduction: From sensing to disease and treatment. Trends Pharmacol Sci 2001; 22:254–260.
Sigurdson W, Ruknudin A, Sachs F. Calcium imaging of mechanically induced fluxes in tissue-cultured chick heart: Role of stretch-activated ion channels. Am J Physiol 1992; 262:H1110–H1115.
Sadoshima J, Izumo S. The cellular and molecular response of cardiac myocytes to mechanical stress. Annu Rev Physiol 1997; 59:551–571.
Laine M, Id L, Vuolteenaho O et al. Role of calcium in stretch-induced release and mRNA synthesis of natriuretic peptides in isolated rat atrium. Pflugers Arch 1996; 432:953–960.
Parsons JT. Integrin-mediated signalling: Regulation by protein tyrosine kinases and small GTP-binding proteins. Curr Opin Cell Biol 1996; 8:146–152.
Liang F, Atakilit A, Gardner DG. Integrin dependence of brain natriuretic peptide gene promoter activation by mechanical strain. J Biol Chem 2000a; 275:20355–20360.
Aikawa R, Nagai T, Kudoh S et al. Integrins play a critical role in mechanical stress-induced p38 MAPK activation. Hypertension 2002; 39:233–238.
Brancaccio M, Fratta L, Notte A et al. Melusin, a muscle-specific integrin beta 1-interacting protein, is required to prevent cardiac failure in response to chronic pressure overload. Nat Med 2003; 9:68–75.
Nishizuka Y. Turnover of inositol phospholipids and signal transduction. Science 1984; 225:1365–1370.
Nishizuka Y. Studies and perspectives of protein kinase C. Science 1986; 233:305–312.
van Biesen T, Hawes BE, Luttrell DK et al. Receptor-tyrosine-kinase-and G beta gamma-mediated MAP kinase activation by a common signalling pathway. Nature 1995; 376:781–784.
Thuerauf DJ, Glembotski CC. Differential effects of protein kinase C, Ras, and Raf-1 kinase on the induction of the cardiac B-type natriuretic peptide gene through a critical promoter-proximal M-CAT element. J Biol Chem 1997; 272:7464–7472.
Sugden PH, Clerk A. Cellular mechanisms of cardiac hypertrophy. J Mol Med 1998; 76:725–746.
Yamazaki T, Komuro I, Kudoh S et al. Mechanical stress activates protein kinase cascade of phosphorylation in neonatal rat cardiac myocytes. J Clin Invest 1995b; 96:438–446.
Liang F, Gardner DG. Mechanical strain activates BNP gene transcription through a p38/NF-kappaB-dependent mechanism. J Clin Invest 1999; 104:1603–1612.
Liang F, Lu S, Gardner DG. Endothelin-dependent and-independent components of strain-activated brain natriuretic peptide gene transcription require extracellular signal regulated kinase and p38 mitogen-activated protein kinase. Hypertension 2000b; 35:188–192.
Pikkarainen S, Tokola H, Kerkelä R et al. Endothelin-1 specific activation of B-type natriuretic peptide gene via p38 mitogen activated protein kinase and nuclear ETS factors. J Biol Chem 2002b.
Molkentin JD. The zinc finger-containing transcription factors GATA-4,-5, and-6. Ubiquitously expressed regulators of tissue-specific gene expression. J Biol Chem 2000a; 275:38949–38952.
Emery JG, Ohlstein EH, Jaye M. Therapeutic modulation of transcription factor activity. Trends Pharmacol Sci 2001; 22:233–240.
Grepin C, Dagnino L, Robitaille L et al. A hormone-encoding gene identifies a pathway for cardiac but not skeletal muscle gene transcription. Mol Cell Biol 1994; 14:3115–3129.
Thuerauf DJ, Hanford DS, Glembotski CC. Regulation of rat brain natriuretic peptide transcription. A potential role for GATA-related transcription factors in myocardial cell gene expression. J Biol Chem 1994; 269:17772–17775.
Lapointe MC, Wu G, Garami M et al. Tissue-specific expression of the human brain natriuretic peptide gene in cardiac myocytes. Hypertension 1996; 27:715–722.
He Q, Mendez M, Lapointe MC. Regulation of the human brain natriuretic peptide gene by GATA-4. Am J Physiol Endocrinol Metab 2002; 283:E50–E57.
Marttila M, Hautala N, Paradis P et al. GATA4 mediates activation of the B-type natriuretic peptide gene expression in response to hemodynamic stress. Endocrinology 2001; 142:4693–4700.
Ogawa E, Saito Y, Kuwahara K et al. Fibronectin signaling stimulates BNP gene transcription by inhibiting neuron-restrictive silencer element-dependent repression. Cardiovasc Res 2002; 53:451–459.
Herzig TC, Jobe SM, Aoki H et al. Angiotensin II type1a receptor gene expression in the heart: AP-1 and GATA-4 participate in the response to pressure overload. Proc Natl Acad Sci USA 1997; 94:7543–7548.
Hasegawa K, Lee SJ, Jobe SM et al. cis-Acting sequences that mediate induction of beta-myosin heavy chain gene expression during left ventricular hypertrophy due to aortic constriction [see comments]. Circulation 1997; 96:3943–3953.
Hautala N, Tokola H, Luodonpää M et al. Pressure overload increases GATA4 binding activity via endothelin-1. Circulation 2001; 103:730–735.
Hautala N, Tenhunen O, Szokodi I et al. Direct left ventricular wall stretch activates GATA4 binding in perfused rat heart: Involvement of autocrine/paracrine pathways. Pflugers Arch 2002; 443:362–369.
Liang Q, Wiese RJ, Bueno OF et al. The transcription factor GATA4 is activated by extracellular signal-Regulated kinase 1-and 2-mediated phosphorylation of serine 105 in cardiomyocytes. Mol Cell Biol 2001b; 21:7460–7469.
Pikkarainen S, Kerkelä R, Pöntinen J et al. Decoy oligonucleotide characterization of GATA-4 transcription factor in hypertrophic agonist induced responses of cardiac myocytes. J Mol Med 2002a; 80:51–60.
Charron F, Tsimiklis G, Arcand M et al. Tissue-specific GATA factors are transcriptional effectors of the small GTPase RhoA. Genes Dev 2001; 15:2702–2719.
Kerkelä R, Pikkarainen S, Majalahti-Palviainen T et al. Distinct roles of mitogen activated protein kinase pathways in GATA-4 transcription factor mediated regulation of B-type natriuretic peptide gene. J Biol Chem 2002; 277:13752–13760.
Liang Q, De Windt LJ, Witt SA et al. The transcription factors GATA4 and GATA6 regulate cardiomyocyte hypertrophy in vitro and in vivo. J Biol Chem 2001a; 276:30245–30253.
Kim Y, Ma AG, Kitta K et al. Anthracycline-induced suppression of GATA-4 transcription factor: Implication in the regulation of cardiac myocyte apoptosis. Mol Pharmacol 2003; 63:368–377.
Durocher D, Charron F, Warren R et al. The cardiac transcription factors Nkx2-5 and GATA-4 are mutual cofactors. EMBO J 1997; 16:5687–5696.
Molkentin JD, Lu JR, Antos CL et al. A calcineurin-dependent transcriptional pathway for cardiac hypertrophy. Cell 1998; 93:215–228.
Belaguli NS, Sepulveda JL, Nigam V et al. Cardiac tissue enriched factors serum response factor and GATA-4 are mutual coregulators. Mol Cell Biol 2000; 20:7550–7558.
Morin S, Charron F, Robitaille L et al. GATA-dependent recruitment of MEF2 proteins to target promoters. EMBO J 2000; 19:2046–2055.
Bhalla SS, Robitaille L, Nemer M. Cooperative activation by GATA-4 and YY1 of the cardiac B-type natriuretic peptide promoter. J Biol Chem 2001; 276:11439–11445.
Dai YS, Cserjesi P, Markham BE et al. The transcription factors GATA4 and dHAND physically interact to synergistically activate cardiac gene expression through a p300-Dependent mechanism. J Biol Chem 2002; 277:24390–24398.
Charron F, Paradis P, Bronchain O et al. Cooperative interaction between GATA-4 and GATA-6 regulates myocardial gene expression. Mol Cell Biol 1999; 19:4355–4365.
Tevosian SG, Deconinck AE, Cantor AB et al. FOG-2: A novel GATA-family cofactor related to multitype zinc-finger proteins Friend of GATA-1 and U-shaped. Proc Natl Acad Sci USA 1999; 96:950–955.
Hardt SE, Sadoshima J. Glycogen synthase kinase-3beta: A novel regulator of cardiac hypertrophy and development. Circ Res 2002; 90:1055–1063.
Morisco C, Seta K, Hardt SE et al. Glycogen synthase kinase 3beta regulates GATA4 in cardiac myocytes. J Biol Chem 2001; 276:28586–28597.
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Pikkarainen, S., Tokola, H., Ruskoaho, H. (2007). Mechanotransduction of the Endocrine Heart. In: Cardiac Mechanotransduction. Springer, New York, NY. https://doi.org/10.1007/978-0-387-48868-4_9
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