Abstract
The theme of this book is vascular remodeling, and perhaps one reason why this concept is of current interest is because our knowledge of arterial lesion growth in experimental animals after angioplasty has not been predicative of the process of lesion growth in humans. In particular, agents found to be important in inhibiting lesions in small mammalian arteries after balloon injury have not been useful in predicting the outcomes in humans after angioplasty (1). One possibility, therefore, is that the growth of lesions in humans does not involve those cellular processes which occur in the rat artery. The role of this chapter is to try to point out some of the differences that may have been responsible for this belief and to highlight the key molecular events that are known to take place in lesion growth in our experimental models.
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References
MERCATOR Study Group. 1992. Does the new angiotensin converting enzyme inhibitor cilazapril prevent restenosis after percutaneous transluminal coronary angioplasty? Circulation. 86:100–110.
Austin, G. E., N. B. Ratliff, J. Holtman, S. Tabei, and D. F. Phillips. 1985. Intimal proliferation of smooth muscle cells as an explanation for recurrent coronary artery stenosis after percutaneous transluminal coronary angioplasty. Journal Of The American College Of Cardiology. 6:369–375.
Waller, B. F., C. A. Pinkerton, and L. N. Foster. 1987. Morphologic evidence of accelerated left main coronary artery stenosis: a late complication of percutaneous transluminal balloon angioplasty of the proximal left anterior descending coronary artery. Journal Of The American College Of Cardiology. 9:1019–1023.
Liu, M. W., G. S. Roubin, and S. B. King. 1989. Restenosis after coronary angioplasty. Potential biologic determinants and role of intimai hyperplasia. Circulation. 79:1374–1387.
Clowes, A. W., M. A. Reidy, and M. M. Clowes. 1983. Kinetics of cellular proliferation after arterial injury. I. Smooth muscle growth in the absence of endothelium. Lab. Invest. 49:327–333.
Clowes, A. W., M. A. Reidy, and M. M. Clowes. 1983. Mechanisms of stenosis after arterial injury. Lab. Invest. 49:208–215.
Lafont, A., Durand E., Rabat, S., de Oliveira, M., Guérin, Y., Fernandez, F., Desnos, M., and Guérot, C. 1995. [Restenosis: physiopathology, treatments and prevention]. Ann. Cardiol. Angeiol. 44:349–353.
Laurent, S., Vanhoutte, P., Cavero, I., and et al. 1995. [Arterial wall: a new pharmacological and therapeutic target?]. Therapie. 50:387–398.
Basso, C., A. Angelini, and G. Thiene. 1994. [Histopathological features of balloon coronary angioplasty]. Cardiologia. 39:47–51.
Schwartz, R. S. 1994. Neointima and arterial injury: dogs, rats, pigs, and more [editorial; comment]. Lab Invest. 71:789–791.
Glagov, S., E. Weisenberg, C. K. Zarins, R. Stankunavicius, and G. J. Kolettis. 1987. Compensatory enlargement of human atherosclerotic coronary arteries. New Eng J Med. 316:1371–1375.
Folkow, B. 1982. Physiological aspects of primary hypertension. Physiol Rev. 62:347–504.
Jamal, A., M. Bendeck, and B. L. Langille. 1992. Structural changes and recovery of function after arterial injury. Arterioscler. Thromb. 12:307–317.
Langille, B. L. and F. O’donnell. 1986. Reductions in arterial diameter produced by chronic decreases in blood flow are endothelium-dependent. Science 231:405–407.
Cho, A., D. W. Courtman, and B. L. Langille. 1995. Apoptosis (programmed cell death) in arteries of the neonatal lamb. Circ Res. 76:168–175.
Langille, B. L. 1991. Hemodynamic factors and vascular disease. In Cardiovascular pathology. M.D. Silver, editor. Churchill Livingstone, New York, New York. 131–154.
Nobuyoshi, M., T. Kimura, H. Ohishi, H. Horiuchi, H. Nosaka, N. Hamasaki, H. Yokoi, and K. Kim. 1991. Restenosis after percutaneous transluminal coronary angioplasty: pathologic observations in 20 patients. J. Am. Coll. Cardiol. 17:433–439.
Miller, M. J., R. E. Kuntz, S. P. Friedrich, G. A. Leidig, R. F. Fishman, S. J. Schnitt, D. S. Bairn, and R. D. Safian. 1993. Frequency and consequences of intimal hyperplasia in specimens retrieved by directional atherectomy of native primary coronary artery stenoses and subsequent restenoses. Am. J. Cardiol. 71:652–658.
Schnitt, S. J., R. D. Safian, R. E. Kuntz, D. A. Schmidt, and D. S. Bairn. 1992. Histologic findings in specimens obtained by percutaneous directional coronary atherectomy. Human Pathology. 23:415–420.
Orekhov, A. N., I. I. Karpova, V. V. Tertov, S. A. Rudchenko, E. R. Andreeva, A. V. Krushinsky, and V. N. Smimov. 1984. Cellular composition of atherosclerotic and uninvolved human aortic subendothelial intima. Light-microscopic study of dissociated aortic cells. Am JI Pathol. 115:17–24.
Rekhter, M. D., E. R. Andreeva, I. V. Andrianova, A. A. Mironov, and A. N. Orekhov. 1992. Stellate cells of aortic intima: I. Human and rabbit. Tissue Cell 24:689–696.
Andreeva, E. R., M. D. Rekhter, Y. A. Romanov, G. M. Antonova, A. S. Antonov, A. A. Mironov, and A. N. Orekhov. 1992. Stellate cells of aortic intima: II. Arborization of intima) cells in culture. Tissue Cell 24:697–704.
Fairman, M. P. 1990. DNA polymerase delta/PCNA: actions and interactions. Journal Of Cell Science. 95:1–4.
O’Brien, E. R., C. E. Alpers, D. K. Stewart, M. Ferguson, N. Tran, D. Gordon, E. P. Benditt, T. Hinohara, J. B. Simpson, and S. M. Schwartz. 1993. Proliferation in primary and restenotic coronary atherectomy tissue: Implications for antiproliferative therapy. Circ. Res. 73:223–231.
Leclerc G, Kearney M, Schneider D, Rosenfield K, Losordo DW, and Isner JM. 1993. Assessment of cell kinetics in human restenotic lesions by in vitro bromodeoxyuridine labeling of excised atherectomy specimens. Clin Res 41:343A.
Pickering, J. G., L. Weir, J. Jekanowski, M. A. Kearney, and J. M. Isner. 1993. Proliferative activity in peripheral and coronary atherosclerotic plaque among patients undergoing percutaneous revascularization. J. Clin. Invest. 91:1469–1480.
Clowes, A. W., M. M. Clowes, and M. A. Reidy. 1986. Kinetics of cellular proliferation after arterial injury. Ill. Endothelial and smooth muscle growth in chronically denuded vessels. Lab. Invest. 54:295–303.
Lindner, V. and M. A. Reidy. 1991. Proliferation of smooth muscle cells after vascular injury is inhibited by an antibody against basic fibroblast growth factor. Proc. Natl. Acad. Sci. USA 88:3739–3743.
Olson, N. E., S. Chao, V. Lindner, and M. A. Reidy. 1992. Intimal smooth muscle cell proliferation after balloon catheter injury: The role of basic fibroblast growth factor. Am. J. Pathol. 140:1017–1023.
Fingerle, J., R. M. K. Müller, H. Kuhn, M. Pech, and H. R. Baumgartner. 1995. Mechanism of inhibition of neointimal formation by the angiotensin-converting enzyme inhibitor cilazapril - A study in balloon catheter-injured rat carotid arteries. Arterioscler. Thromb. Vasc. Biol. 15:1945–1950.
Lindner, V., N. E. Olson, A. W. Clowes, and M. A. Reidy. 1992. Inhibition of smooth muscle cell proliferation in injured rat arteries. Interaction of heparin with basic fibroblast growth factor. J. Clin. Invest. 90:2044–2049.
Riessen, R., T. N. Wight, C. Pastore, C. Henley, and J. M. Isner. 1996. Distribution of hyaluronan during extracellular matrix remodeling in human restenotic arteries and balloon-injured rat carotid arteries. Circulation 93:1141–1147.
Schwartz, S. M., M. R. Reidy, and A. Clowes. 1985. Kinetics of atherosclerosis: a stem cell model. Ann. N. Y. Acad. Sci. 454:292–304.
Jawien, A. D., D. F. Bowen-Pope, V. Lindner, S. M. Schwartz, and A. W. Clowes. 1992. Platelet-derived growth factor promotes smooth muscle migration and intimai thickening in a rat model of balloon angioplasty. J. Clin. Invest. 89:507–511.
Bendeck, M. P., N. Zempo, A. W. Clowes, R. E. Galardy, and M. A. Reidy. 1994. Smooth muscle cell migration and matrix metalloproteinase expression after arterial injury in the rat. Circ. Res. 75:539–545.
Fingerle, J., R. Johnson, A. W. Clowes, M. W. Majesky, and M. A. Reidy. 1989. Role of platelets in smooth muscle cell proliferation and migration after vascular injury in rat carotid artery. Proc. Natl. Acad. Sci. USA 86:8412–8416.
Jackson, C. L. and M. A. Reidy. 1993. Basic fibroblast growth factor: Its role in the control of smooth muscle cell migration. Am. J. Pathol. 143:1024–1031.
Jackson, C. L., E. Raines, R. Ross, and M. A. Reidy. 1993. Role of endogenous platelet-derived growth factor in arterial smooth muscle cell migration after balloon catheter injury. Arterioscler. Thromb. Vasc. Biol 13:1218–1226.
Clowes, A. W., M. M. Clowes, T. R. Kirkman, C. L. Jackson, Y. P. T. Au, and R. Kenagy. 1992. Heparin inhibits the expression of tissue-type plasminogen activator by smooth muscle cells in injured rat carotid artery. Circ. Res. 70:1128–1136.
Clowes, A. W. and M. J. Karnowsky. 1977. Suppression by heparin of smooth muscle cell proliferation in injured arteries. Nature 265:625–626.
Birkedal Hansen, H., W. G. Moore, M. K. Bodden, L. J. Windsor, B. Birkedal Hansen, A. DeCarlo, and J. A. Engler. 1993. Matrix metalloproteinases: a review. Critical Rev Oral Biol Med. 4:197–250.
Murphy, G., J. J. Reynolds, and R. M. Hembry. 1989. Metalloproteinases and cancer invasion and metastasis. Int. J Cancer 44:757–760.
Bendeck, M. P., C. Irvin, and M. A. Reidy. 1996. Inhibition of matrix metalloproteinase activity inhibits smooth muscle cell migration but not neointimal thickening after arterial injury. Circ. Res. 78:38–43.
Koyama, H. and M. A. Reidy. 1996. Reinjury of arterial intimai lesions induces smooth muscle cell replication which is not controlled by fibroblast growth factor 2. Circ Res. (In Press)
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Reidy, M.A. (1997). Intimal Lesion Growth: An Assessment of Important Cellular Events. In: Lafont, A., Topol, E.J. (eds) Arterial Remodeling: A Critical Factor in Restenosis. Developments in Cardiovascular Medicine, vol 198. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-6079-1_17
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DOI: https://doi.org/10.1007/978-1-4615-6079-1_17
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