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Alternate-day fasting reverses the age-associated hypertrophy phenotype in rat heart by influencing the ERK and PI3K signaling pathways

Castello, Laura, Maina, Marco, Testa, Gabriella, Cavallini, Gabriella, Biasi, Fiorella, Donati, Alessio, Leonarduzzi, Gabriella, Bergamini, Ettore, Poli, Giuseppe, Chiarpotto, Elena·2011·Mechanisms of Ageing and Development

Abstract

The age-related increased impedance in large arteries overloads the senescent heart, and the myocardial phenotype is hypertrophic. Together with qualitative changes observed in the senile heart, this can be responsible for impaired diastolic function. A restricted diet providing adequate nutrient intake, e.g. alternate-day fasting (ADF), has been shown to extend life-span and decrease incidence and progression of age-associated diseases in laboratory rodents, and to ameliorate some metabolic markers of aging in rhesus monkeys and humans. This study reports an age-related increase of some biological and morphological hypertrophy markers in the rat heart, together with increased plasma BNP, a well known marker of heart failure. The tissue modifications might likely be related to hyper-activation of two of the signaling pathways associated with myocardial pathological hypertrophy: ERK1/2 and PI3Kγ. Increased ERK1/2 activation might be in part related to the disturbance of STAT3, with a consequent decrease of SOCS3. In this context, the down-modulation of ERK1/2 and PI3Kγ signaling, together with the restoration of STAT3 activity and SOCS3 content, both observed with ADF, might help to reduce pathological hypertrophy stimuli and to rescue an important cardioprotective pathway, possibly opening new preventive and therapeutic perspectives in age-related heart failure.

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  • Endurance training and alternate-day-fasting may improve healthspan through their capacity to avoid mitochondrial degeneration.

    “endurance training and alternate-day-fasting may improve healthspan through their capacity to avoid mitochondrial degeneration”

    From The Hallmarks of Aging (2013) · cites this paper as Castello et al., 2011

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Research works printed but not linked: 77

  1. Anderson, 2009, Caloric restriction and aging studies in mice and monkeys, Toxicol. Pathol., 37, 47, 10.1177/0192623308329476 · DOI · Paper page
  2. Anson, 2005, The diet restriction paradigm: a brief review of the effects of every-other-day feeding, Age, 27, 17, 10.1007/s11357-005-3286-2 · DOI
  3. Aoyagi, 2001, Hemodynamic overload-induced activation of myocardial mitogen-activated protein kinases in vivo: augmented responses in young spontaneously hypertensive rats and diminished responses in aged Fischer 344 rats, Hypertension, 37, 52, 10.1161/01.HYP.37.1.52 · DOI
  4. Aronson, 2003, Cross-linking of glycated collagen in the pathogenesis of arterial and myocardial stiffening of aging and diabetes, J. Hypertens., 21, 3, 10.1097/00004872-200301000-00002 · DOI
  5. Berni, 2009, Modulation of actin isoform expression before the transition from experimental compensated pressure-overload cardiac hypertrophy to decompensation, Am. J. Physiol. Heart Circ. Physiol., 296, H1625, 10.1152/ajpheart.01057.2008 · DOI
  6. Boengler, 2008, The myocardial JAK/STAT pathway: from protection to failure, Pharmacol. Ther., 120, 172, 10.1016/j.pharmthera.2008.08.002 · DOI
  7. Booz, 2002, Interplay between the cardiac renin angiotensin system and JAK-STAT signaling: role in cardiac hypertrophy, ischemia/reperfusion dysfunction, and heart failure, J. Mol. Cell. Cardiol., 34, 1443, 10.1006/jmcc.2002.2076 · DOI
  8. Bradford, 1976, A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein–dye binding, Anal. Biochem., 72, 248, 10.1016/0003-2697(76)90527-3 · DOI · Paper page
  9. Bueno, 2000, The MEK1–ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice, EMBO J., 19, 6341, 10.1093/emboj/19.23.6341 · DOI
  10. Carrier, 1992, Expression of the sarcomeric actin isogenes in the rat heart with development and senescence, Circ. Res., 70, 999, 10.1161/01.RES.70.5.999 · DOI
  11. Castello, 2005, Calorie restriction protects against age-related rat aorta sclerosis, FASEB J., 19, 1863, 10.1096/fj.04-2864fje · DOI
  12. Castello, 2010, Alternate-day fasting protects the rat heart against age-induced inflammation and fibrosis by inhibiting oxidative damage and NF-kB activation, Free Radic. Biol. Med., 48, 47, 10.1016/j.freeradbiomed.2009.10.003 · DOI
  13. Cheng, 2009, Mechanism of diastolic stiffening of the failing myocardium and its prevention by angiotensin receptor and calcium channel blockers, J. Cardiovasc. Pharmacol., 54, 47, 10.1097/FJC.0b013e3181ab371d · DOI
  14. Clerk, 2006, Peptide growth factors signal differentially through protein kinase C to extracellular signal-regulated kinases in neonatal cardiomyocytes, Cell Signal., 18, 225, 10.1016/j.cellsig.2005.04.005 · DOI
  15. Colman, 2009, Caloric restriction delays disease onset and mortality in rhesus monkeys, Science, 325, 201, 10.1126/science.1173635 · DOI · Paper page
  16. Dhahbi, 2006, Gene expression and physiologic responses of the heart to the initiation and withdrawal of caloric restriction, J. Gerontol. A: Biol. Sci. Med. Sci., 61, 218, 10.1093/gerona/61.3.218 · DOI
  17. Dolinsky, 2010, Calorie restriction prevents hypertension and cardiac hypertrophy in the spontaneously hypertensive rat, Hypertension, 56, 412, 10.1161/HYPERTENSIONAHA.110.154732 · DOI
  18. Dorn, 2007, II. The fuzzy logic of physiological cardiac hypertrophy, Hypertension, 49, 962, 10.1161/HYPERTENSIONAHA.106.079426 · DOI
  19. Ferrara, 1997, Alterations in beta-adrenoceptor mechanisms in the aging heart. Relationship with heart failure, Aging (Milano), 9, 391
  20. Fischer, 2008, Role of gp130-mediated signalling pathways in the heart and its impact on potential therapeutic aspects, Br. J. Pharmacol., 153, S414
  21. Fredj, 2005, Role of interleukin-6 in cardiomyocyte/cardiac fibroblast interactions during myocyte hypertrophy and fibroblast proliferation, J. Cell. Physiol., 204, 428, 10.1002/jcp.20307 · DOI
  22. Frey, 2004, Hypertrophy of the heart: a new therapeutic target?, Circulation, 109, 1580, 10.1161/01.CIR.0000120390.68287.BB · DOI
  23. Gottdiener, 2000, Predictors of congestive heart failure in the elderly: the cardiovascular health study, J. Am. Coll. Cardiol., 35, 1628, 10.1016/S0735-1097(00)00582-9 · DOI · Paper page
  24. Gradman, 2006, From left ventricular hypertrophy to congestive heart failure: management of hypertensive heart disease, Prog. Cardiovasc. Dis., 48, 326, 10.1016/j.pcad.2006.02.001 · DOI
  25. Hacker, 2006, Age-related changes in cardiac structure and function in Fischer 344×Brown Norway hybrid rats, Am. J. Physiol. Heart Circ. Physiol., 290, H304, 10.1152/ajpheart.00290.2005 · DOI
  26. Hattori, 2001, Role of STAT3 in ischemic preconditioning, J. Mol. Cell Cardiol., 33, 1929, 10.1006/jmcc.2001.1456 · DOI
  27. Heilbronn, 2003, Calorie restriction and aging: review of the literature and implications for studies in humans, Am. J. Clin. Nutr., 78, 361, 10.1093/ajcn/78.3.361 · DOI · Paper page
  28. Heineke, 2006, Regulation of cardiac hypertrophy by intracellular signalling pathways, Nat. Rev. Mol. Cell. Biol., 7, 589, 10.1038/nrm1983 · DOI
  29. Holloszy, 2007, Caloric restriction in humans, Exp. Gerontol., 42, 709, 10.1016/j.exger.2007.03.009 · DOI
  30. Hursting, 2003, Calorie restriction, aging, and cancer prevention: mechanisms of action and applicability to humans, Annu. Rev. Med., 54, 131, 10.1146/annurev.med.54.101601.152156 · DOI
  31. Iemitsu, 2001, Physiological and pathological cardiac hypertrophy induce different molecular phenotypes in the rat, Am. J. Physiol. Regul. Integr. Comp. Physiol., 281, R2029, 10.1152/ajpregu.2001.281.6.R2029 · DOI
  32. Inuzuka, 2009, Suppression of phosphoinositide 3-kinase prevents cardiac aging in mice, Circulation, 120, 1695, 10.1161/CIRCULATIONAHA.109.871137 · DOI
  33. Izumi, 1998, Cardiac mitogen-activated protein kinase activities are chronically increased in stroke-prone hypertensive rats, Hypertension, 31, 50, 10.1161/01.HYP.31.1.50 · DOI
  34. Jacoby, 2003, Cardiomyocyte-restricted knockout of STAT3 results in higher sensitivity to inflammation, cardiac fibrosis, and heart failure with advanced age, Proc. Natl. Acad. Sci. U.S.A., 100, 12929, 10.1073/pnas.2134694100 · DOI · Paper page
  35. Jain, 1998, Repression of STAT3 activity by activation of mitogen-activated protein kinase (MAPK), Oncogene, 17, 3157, 10.1038/sj.onc.1202238 · DOI
  36. Johnston, 2004, Are SOCS suppressors, regulators, and degraders?, J. Leukoc. Biol., 75, 743, 10.1189/jlb.1003507 · DOI
  37. Kass, 2002, Age-related changes in ventricular–arterial coupling: pathophysiologic implications, Heart Fail. Rev., 7, 51, 10.1023/A:1013749806227 · DOI
  38. Kawaguchi, 2003, Combined ventricular systolic and arterial stiffening in patients with heart failure and preserved ejection fraction: implications for systolic and diastolic reserve limitations, Circulation, 107, 714, 10.1161/01.CIR.0000048123.22359.A0 · DOI
  39. Kennedy, 2006, Using U0126 to dissect the role of the extracellular signal-regulated kinase 1/2 (ERK1/2) cascade in the regulation of gene expression by endothelin-1 in cardiac myocytes, J. Mol. Cell. Cardiol., 41, 236, 10.1016/j.yjmcc.2006.04.011 · DOI
  40. Klemola, 1999, Catecholamines in pericardial fluid of normotensive, spontaneously hypertensive and reserpine-treated rats, Acta Physiol. Scand., 165, 293, 10.1046/j.1365-201x.1999.00507.x · DOI
  41. Ko, 2009, Nutrient stress activates inflammation and reduces glucose metabolism by suppressing AMP-activated protein kinase in the heart, Diabetes, 58, 2536, 10.2337/db08-1361 · DOI
  42. Kong, 2005, Genetic expression profiles during physiological and pathological cardiac hypertrophy and heart failure in rats, Physiol. Genomics, 21, 34, 10.1152/physiolgenomics.00226.2004 · DOI
  43. Kopelman, 2007, Health risks associated with overweight and obesity, Obes. Rev., 8, 13, 10.1111/j.1467-789X.2007.00311.x · DOI · Paper page
  44. Kunisada, 2000, Signal transducer and activator of transcription 3 in the heart transduces not only a hypertrophic signal but a protective signal against doxorubicin-induced cardiomyopathy, Proc. Natl. Acad. Sci. U.S.A., 97, 315, 10.1073/pnas.97.1.315 · DOI
  45. Lakatta, 2003, Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises. Part III: cellular and molecular clues to heart and arterial aging, Circulation, 107, 490, 10.1161/01.CIR.0000048894.99865.02 · DOI
  46. Lakatta, 2003, Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises. Part II: the aging heart in health: links to heart disease, Circulation, 107, 346, 10.1161/01.CIR.0000048893.62841.F7 · DOI
  47. Livak, 2001, Analysis of relative gene expression data using real-time quantitative PCR and the 2(−Delta Delta C(T)) method, Methods, 25, 402, 10.1006/meth.2001.1262 · DOI · Paper page
  48. MacLellan, 1994, Transforming growth factor-beta response elements of the skeletal alpha-actin gene. Combinatorial action of serum response factor, YY1, and the SV40 enhancer-binding protein, TEF-1, J. Biol. Chem., 269, 16754, 10.1016/S0021-9258(19)89455-3 · DOI
  49. McKinsey, 2007, Small-molecule therapies for cardiac hypertrophy moving beneath the cell surface, Nat. Rev. Drug Discov., 6, 617, 10.1038/nrd2193 · DOI
  50. McMullen, 2003, Phosphoinositide 3-kinase (p110alpha) plays a critical role for the induction of physiological, but not pathological, cardiac hypertrophy, Proc. Natl. Acad. Sci. U.S.A., 100, 12355, 10.1073/pnas.1934654100 · DOI
  51. Minami, 2000, Effect of a hypocaloric diet on adrenomedullin and natriuretic peptides in obese patients with essential hypertension, J. Cardiovasc. Pharmacol., 36, S83, 10.1097/00005344-200000006-00018 · DOI
  52. Nascimento, 2008, Misclassification probability as obese or lean in hypercaloric and normocaloric diet, Biol. Res., 41, 253, 10.4067/S0716-97602008000300002 · DOI
  53. Ni, 2003, Shear flow attenuates serum-induced STAT3 activation in endothelial cells, J. Biol. Chem., 278, 19702, 10.1074/jbc.M300893200 · DOI
  54. Niemann, 2010, Caloric restriction delays cardiac ageing in rats: role of mitochondria, Cardiovasc. Res., 88, 267, 10.1093/cvr/cvq273 · DOI
  55. Nishikawa, 2006, Left ventricular hypertrophy in mice with a cardiac-specific overexpression of interleukin-1, Am. J. Physiol. Heart Circ. Physiol., 291, H176, 10.1152/ajpheart.00269.2005 · DOI
  56. Okin, 2007, Regression of electrocardiographic left ventricular hypertrophy is associated with less hospitalization for heart failure in hypertensive patients, Ann. Intern. Med., 147, 311, 10.7326/0003-4819-147-5-200709040-00006 · DOI
  57. O’Neill, 2005, Akt1 in the cardiovascular system: friend or foe?, J. Clin. Invest., 115, 2059, 10.1172/JCI25900 · DOI
  58. Osadchii, 2007, Rat strain-related differences in myocardial adrenergic tone and the impact on cardiac fibrosis, adrenergic responsiveness and myocardial structure and function, Pharmacol. Res., 55, 287, 10.1016/j.phrs.2006.12.005 · DOI
  59. Parker, 1990, Peptide growth factors can provoke “fetal” contractile protein gene expression in cardiac myocytye hypertrophy, J. Clin. Invest., 85, 507, 10.1172/JCI114466 · DOI
  60. Patrucco, 2004, PI3Kgamma modulates the cardiac response to chronic pressure overload by distinct kinase-dependent and -independent effects, Cell, 118, 375, 10.1016/j.cell.2004.07.017 · DOI
  61. Peterson, 1983, Determination of total protein, Methods Enzymol., 91, 95, 10.1016/S0076-6879(83)91014-5 · DOI
  62. Podewski, 2003, Alterations in Janus kinase (JAK)-signal transducers and activators of transcription (STAT) signaling in patients with end-stage dilated cardiomyopathy, Circulation, 107, 798, 10.1161/01.CIR.0000057545.82749.FF · DOI
  63. Redman, 2007, Effect of calorie restriction with or without exercise on body composition and fat distribution, J. Clin. Endocrinol. Metab., 92, 865, 10.1210/jc.2006-2184 · DOI · Paper page
  64. Schwartz, 1986, α-Skeletal muscle actin mRNA's accumulate in hypertrophied adult rat hearts, Circ. Res., 59, 551, 10.1161/01.RES.59.5.551 · DOI
  65. Smith, 2004, Genetic depletion of cardiac myocyte STAT-3 abolishes classical preconditioning, Cardiovasc. Res., 63, 611, 10.1016/j.cardiores.2004.06.019 · DOI · Paper page
  66. Stauss, 1995, Does low frequency power of arterial blood pressure reflect sympathetic tone?, J. Auton. Nerv. Syst., 54, 145, 10.1016/0165-1838(94)00000-A · DOI
  67. Stern, 2001, Calorie restriction in obesity: prevention of kidney disease in rodents, J. Nutr., 131, 913S, 10.1093/jn/131.3.913S · DOI
  68. Stilli, 2006, Correlation of alpha-skeletal actin expression, ventricular fibrosis and heart function with the degree of pressure overload cardiac hypertrophy in rats, Exp. Physiol., 91, 571, 10.1113/expphysiol.2005.032607 · DOI
  69. Suurmeijer, 2003, α-Actin isoform distribution in normal and failing human heart: a morphological, morphometric, and biochemical study, J. Pathol., 199, 387, 10.1002/path.1311 · DOI
  70. Susic, 2008, The aging hypertensive heart: a brief update, Nat. Clin. Pract. Cardiovasc. Med., 5, 104, 10.1038/ncpcardio1091 · DOI
  71. Vesely, 2009, Cardiac natriuretic peptides gene expression and secretion in inflammation, J. Investig. Med., 57, 29, 10.2310/JIM.0b013e3181948b37 · DOI
  72. Walford, 2002, Calorie restriction in biosphere 2: alterations in physiologic, hematologic, hormonal, and biochemical parameters in humans restricted for a 2-year period, J. Gerontol. A Biol. Sci. Med. Sci., 57, B211, 10.1093/gerona/57.6.B211 · DOI
  73. Wan, 2003, Intermittent food deprivation improves cardiovascular and neuroendocrine responses to stress in rats, J. Nutr., 133, 1921, 10.1093/jn/133.6.1921 · DOI
  74. Weber, 2000, Fibrosis and hypertensive heart disease, Curr. Opin. Cardiol., 15, 264, 10.1097/00001573-200007000-00010 · DOI
  75. Weindruch, 1997, Seminars in medicine of the Beth Israel Deaconess Medical Center. Caloric intake and aging, N. Engl. J. Med., 337, 986, 10.1056/NEJM199710023371407 · DOI
  76. Yaspelkis, 2010, Aerobic training reverses high-fat diet-induced pro-inflammatory signalling in rat skeletal muscle, Eur. J. Appl. Physiol., 110, 779, 10.1007/s00421-010-1559-7 · DOI
  77. Yasukawa, 2001, Suppressor of cytokine signaling-3 is a biomechanical stress-inducible gene that suppresses gp130-mediated cardiac myocyte hypertrophy and survival pathways, J. Clin. Invest., 108, 1459, 10.1172/JCI13939 · DOI

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Metadata

Authors
Castello, L., Maina, M., Testa, G., Cavallini, G., Biasi, F., Donati, A., Leonarduzzi, G., Bergamini, E., Poli, G., & Chiarpotto, E.
Venue
Mechanisms of Ageing and Development
Publisher
Elsevier BV
Published
2011-06
Volume
132
Issue
6-7
Pages
305-314
ISSN
0047-6374
Cited by
34
References
3
Language
en

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