Summary
Mast cells are known to store and release a variety of biologically active mediators including TNF-α, and proteases such as tryptase and chymase. With cardiac chamber distension there is a release of atrial natriuretic peptide, which is known to cause mast cell degranulation (Figure 2). Secreted TNF-α tryptase and chymase are all capable of activating matrix metalloproteinases, which in turn are responsible for fibrillar collagen degradation. Since one of the roles of the extracellular collagen matrix is to maintain ventricular size and shape, its disruption results in adverse remodeling. Also secreted from the mast cell is a yet to be identified substance that stimulates the maturation of resident immature mast cells. Proof of mast cell involvement in these processes is provided by the use of mast cell membrane stabilizing compounds such as cromolyn sodium, which prevent mast cell degranulation. These drugs prevent the activation of MMPs, degradation of collagen, the increase in mast cell density, adverse ventricular remodeling, and the decrease in contractility as well as attenuate the morbidity/mortality associated with chronic volume overload. They are similarly efficacious in preventing the onset of heart failure in hearts subjected to chronic pressure overload. Finally, evidence is rapidly emerging which identifies mast cell-derived TNF-α and/or the downstream cytokine cascade it induces as a major contributor to adverse ventricular remodeling and associated contractile dysfunction.
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References
Grossman, W., D. Jones, and L.P. McLaurin, Wall stress and patterns of hypertrophy in the human left ventricle. J Clin Invest, 1975. 56: p. 56–64.
Pfeffer, J.M., et al., Progressive ventricular remodeling in rat with myocardial infarction. Am J Physiol, 1991. 260: p. H1406–14.
Borg, T.K. and J.B. Caulfield, The collagen matrix of the heart. Fed Proc, 1981. 40: p. 2037–41.
Robinson, T.F., et al., Structure and function of connective tissue in cardiac muscle: collagen types I and III in endomysial struts and pericellular fibers. Scanning Microsc, 1988. 2: p. 1005–15.
Montfort, I. and R. Perez-Tamayo, The distribution of collagenase in normal rat tissues. J Histochem Cytochem, 1975. 23: p. 910–20.
Lees, M., D.J. Taylor, and D.E. Woolley, Mast cell proteinases activate precursor forms of collagenase and stromelysin, but not of gelatinases A and B. Eur J Biochem, 1994. 223: p. 171–7.
Marone, G., et al., Immunological modulation of human cardiac mast cells. Neurochem Res, 1999. 24: p. 1195–202.
Metcalfe, D.D., D. Baram, and Y.A. Mekori, Mast cells. Physiol Rev, 1997. 77: p. 1033–79.
Nagase, H., Activation mechanisms of matrix metalloproteinases. Biol Chem, 1997. 378: p. 151–60.
Frangogiannis, N.G., et al., Resident cardiac mast cells degranulate and release preformed TNF-alpha, initiating the cytokine cascade in experimental canine myocardial ischemia/reperfusion. Circulation, 1998. 98: p. 699–710.
Suzuki, K., et al., Activation of precursors for matrix metalloproteinases 1 (interstitial collagenase) and 3 (stromelysin) by rat mast-cell proteinases I and II. Biochem J, 1995. 305: p. 301–6.
Patella, V., et al., Increased cardiac mast cell density and mediator release in patients with dilated cardiomyopathy. Inflamm Res, 1997. 46: p. S31–2.
Patella, V., et al., Stem cell factor in mast cells and increased mast cell density in idiopathic and ischemic cardiomyopathy. Circulation, 1998. 97: p. 971–8.
Hara, M., et al., Evidence for a role of mast cells in the evolution to congestive heart failure. J Exp Med, 2002. 195: p. 375–81.
Olivetti, G., et al., Long-term pressure-induced cardiac hypertrophy: capillary and mast cell proliferation. Am J Physiol, 1989. 257: p. H1766–72.
Panizo, A., et al., Are mast cells involved in hypertensive heart disease? J Hypertens, 1995. 13: p. 1201–8.
Engels, W., et al., Transmural changes in mast cell density in rat heart after infarct induction in vivo. J Pathol, 1995. 177: p. 423–9.
Brower, G.L., et al., Cause and effect relationship between myocardial mast cell number and matrix metalloproteinase activity. Am J Physiol, 2002. 283: p. H518–25.
Henegar, J.R. et al., Myocardial Mast Cell Response to Chronic Ventricular Volume Overload. J Mol Cell Cardiol, 1996. 28: p. A202.
Dell’Italia, L.J., et al., Volume-overload cardiac hypertrophy is unaffected by ACE inhibitor treatment in dogs. Am J Physiol, 1997. 273: p. H961–70.
Stewart, J. A., et al., Cardiac mast cell-and chymase-mediated matrix metalloproteinase activity and left ventricular remodeling in mitral regurgitation in the dog. J Mol Cell Cardiol, 2003. 35: p. 311–9.
Estensen, R.D., Eosinophilic myocarditis: a role for mast cells? Arch Pathol Lab Med, 1984. 108: p. 358–9.
Fernex, M., The Mast-Cell System: Its Relationship to Atherosclerosis, Fibrosis and Eosinophils. Baltimore: The Williams & Wilkins Company, 1968: p. 93–95.
Dvorak, A.M., Mast-cell degranulation in human hearts. N Engl J Med, 1986. 315: p. 969–70.
Li, Q.Y., et al., The relationship of mast cells and their secreted products to the volume of fibrosis in posttransplant hearts. Transplantation, 1992. 53: p. 1047–51.
Kovanen, P.T., Role of mast cells in atherosclerosis. Chem Immunol, 1995. 62: p. 132–70.
Galli, S. J., The Paul Kallos Memorial Lecture. The mast cell: a versatile effector cell for a challenging world. Int Arch Allergy Immunol, 1997. 113: p. 14–22.
Patella, V., et al., Human heart mast cells: a definitive case of mast cell heterogeneity. Int Arch Allergy Immunol, 1995. 106: p. 386–93.
Patella, V., et al., Human heart mast cells. Isolation, purification, ultrastructure, and immunologic characterization. J Immunol, 1995. 154: p. 2855–65.
Brownell, E., et al., Immunolocalization of stromelysin-related protein in murine mast cell granules. Int Arch Allergy Immunol, 1995. 107: p. 333–5.
Chancey, A.L., G.L. Brower, and J.S. Janicki, Cardiac mast cell-mediated activation of gelatinase and alteration of ventricular diastolic function. Am J Physiol, 2002. 282: p. H2152–8.
MacKenna, D.A., et al.,Contribution of collagen matrix to passive left ventricular mechanics in isolated rat hearts. Am J Physiol, 1994. 266: p. H1007–18.
Gunja-Smith, Z., et al., Remodeling of human myocardial collagen in idiopathic dilated cardiomyopathy. Role of metalloproteinases and pyridinoline cross-links. Am J Pathol, 1996. 148: p. 1639–48.
Thomas, C.V., et al., Increased matrix metalloproteinase activity and selective upregulation in LV myocardium from patients with end-stage dilated cardiomyopathy. Circulation, 1998. 97: p. 1708–15.
Dixon, I.M., et al., Cardiac collagen remodeling in the cardiomyopathic Syrian hamster and the effect of losartan. J Mol Cell Cardiol, 1997. 29: p. 1837–50.
Janicki, J.S. el al., Interstitial Collagen Remodeling in Chronic Heart Failure. Basic Applied Myology, 1995. 5: p. 339–48.
Spinale, F.G., et al., Cellular and extracellular remodeling with the development and recovery from tachycardia-induced cardiomyopathy: changes in fibrillar collagen, myocyte adhesion capacity and proteoglycans. J Mol Cell Cardiol, 1996. 28: p. 1591–608.
Brower, G.L., J.R. Henegar, and J.S. Janicki, Temporal evaluation of left ventricular remodeling and function in rats with chronic volume overload. Am J Physiol, 1996. 271: p. H2071–8.
Brower, G.L. and J.S. Janicki, Contribution of ventricular remodeling to pathogenesis of heart failure in rats. Am J Physiol, 2001. 280: p. H674–83.
Brower, G.L., W.D. Berry, and J. Janicki, Pharmacologic Inhibition of Mast Cell Degranulation Prevents Left Ventricular Remodeling Induced by Chronic Volume Overload in Rats. Circulation, 1997. 96:p. I–519.
Combs, J.W., D. Lagunoff, and E.P. Benditt, Differentiation and proliferation of embryonic mast cells of the rat. J Cell Biol, 1965. 25: p. 577–92.
Yong, L.C., S. Watkins, and D.L. Wilhelm, The mast cell: distribution and maturation in the peritoneal cavity of the adult rat. Pathology, 1975. 7: p. 307–18.
Yong, L.C., S.G. Watkins, and J.E. Boland, The mast cell: III. Distribution and maturation in various organs of the young rat. Pathology, 1979. 11: p. 427–45.
Marshall, J.S., et al., The role of mast cell degranulation products in mast cell hyperplasia. I. Mechanism of action of nerve growth factor. J Immunol, 1990. 144: p. 1886–92.
Huang, M., R.L. Hester, and A.C. Guyton, Hemodynamic changes in rats after opening an arteriovenous fistula. Am J Physiol, 1992. 262: p. H846–51.
Opgenorth, T.J., et al., Atrial peptides induce mast cell histamine release. Peptides, 1990. 11: p. 1003–7.
Yoshida, H., et al., Histamine release induced by human natriuretic peptide from rat peritoneal mast cells. Regul Pept, 1996. 61: p. 45–9.
Bozkurt, B., et al., Pathophysiologically relevant concentrations of tumor necrosis factor-alpha promote progressive left ventricular dysfunction and remodeling in rats. Circulation, 1998. 97: p. 1382–91.
Bradham, W.S., et al., TNF-alpha and myocardial matrix metalloproteinases in heart failure: relationship to LV remodeling. Am J Physiol, 2002. 282: p. H1288–95.
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Janicki, J.S., Brower, G.L., Chancey, A.L., Forman, M.F., Jobe, L.J. (2005). Cardiac Mast Cells as Mediators of Ventricular Remodeling. In: Villarreal, F.J. (eds) Interstitial Fibrosis in Heart Failure. Developments in Cardiovascular Medicine, vol 253. Springer, New York, NY. https://doi.org/10.1007/0-387-22825-X_10
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