on June 10, 2004
Published online before print June 10, 2004, doi: 10.1161/01.ATV.0000135322.78008.55
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on March 2, 2004
Accepted on June 2, 2004
Proteolysis of the Pericellular Matrix. A Novel Element Determining Cell Survival and Death in the Pathogenesis of Plaque Erosion and Rupture
Ken A. Lindstedt ;
From Wihuri Research Institute, Helsinki, Finland.
* To whom correspondence should be addressed. E-mail: petri.kovanen{at}wri.fi.
Abstract--The 2 major general concepts about the cell biology of atherogenesis, growth of smooth muscle cells, and lipid accumulation in macrophages, ie, foam cell formation, have not been able to satisfactorily explain the genesis of acute coronary syndromes. Rather, the basic pathology behind the acute atherothrombotic events relates to erosion and rupture of unstable coronary plaques. At the cellular level, we now understand that a switch from cellular growth to cellular death, notably apoptosis, could be involved in turning at least some types of atherosclerotic plaques unstable. Because intimal cells require a proper matrix environment for normal function and survival, the vulnerability of an atherosclerotic plaque may critically depend on the integrity of the pericellular matrix of the plaque cells. In vitro studies have revealed that plaque-infiltrating inflammatory cells, such as macrophages, T-lymphocytes, and mast cells, by secreting a variety of proteases capable of degrading pericellular matrix components, induce death of endothelial cells and smooth muscle cells, and so provide a mechanistic explanation for inflammation-dependent plaque erosion and rupture. Thus, a novel link between inflammation and acute coronary syndromes is emerging. For a more explicit understanding of the role of proteases released by inflammatory cells in the conversion of a clinically silent plaque into a dangerous and potentially killing plaque, animal models of plaque erosion and rupture need to be established.
This article has been cited by other articles:
 |
|
 |
|
  R. de Nooijer, I. Bot, J.H. von der Thusen, M.A. Leeuwenburgh, H.S. Overkleeft, A.O. Kraaijeveld, R. Dorland, P.J. van Santbrink, S.H. van Heiningen, M.M. Westra, et al. Leukocyte Cathepsin S Is a Potent Regulator of Both Cell and Matrix Turnover in Advanced Atherosclerosis Arterioscler Thromb Vasc Biol, February 1, 2009; 29(2): 188 - 194. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Lee-Rueckert, R. Vikstedt, J. Metso, M. Jauhiainen, and P. T. Kovanen Association of cholesteryl ester transfer protein with HDL particles reduces its proteolytic inactivation by mast cell chymase J. Lipid Res., February 1, 2008; 49(2): 358 - 368. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Myoishi, H. Hao, T. Minamino, K. Watanabe, K. Nishihira, K. Hatakeyama, Y. Asada, K.-i. Okada, H. Ishibashi-Ueda, G. Gabbiani, et al. Increased Endoplasmic Reticulum Stress in Atherosclerotic Plaques Associated With Acute Coronary Syndrome Circulation, September 11, 2007; 116(11): 1226 - 1233. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. O. Platt, R. F. Ankeny, G.-P. Shi, D. Weiss, J. D. Vega, W. R. Taylor, and H. Jo Expression of cathepsin K is regulated by shear stress in cultured endothelial cells and is increased in endothelium in human atherosclerosis Am J Physiol Heart Circ Physiol, March 1, 2007; 292(3): H1479 - H1486. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Secchiero, R. Candido, F. Corallini, S. Zacchigna, B. Toffoli, E. Rimondi, B. Fabris, M. Giacca, and G. Zauli Systemic Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Delivery Shows Antiatherosclerotic Activity in Apolipoprotein E-Null Diabetic Mice Circulation, October 3, 2006; 114(14): 1522 - 1530. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Sasaki, M. Kuzuya, K. Nakamura, X. W. Cheng, T. Shibata, K. Sato, and A. Iguchi A Simple Method of Plaque Rupture Induction in Apolipoprotein E-Deficient Mice Arterioscler Thromb Vasc Biol, June 1, 2006; 26(6): 1304 - 1309. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Sato, A. Niessner, S. L. Kopecky, R. L. Frye, J. J. Goronzy, and C. M. Weyand TRAIL-expressing T cells induce apoptosis of vascular smooth muscle cells in the atherosclerotic plaque J. Exp. Med., January 23, 2006; 203(1): 239 - 250. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. M Carter Inflammation, thrombosis and acute coronary syndromes Diabetes and Vascular Disease Research, October 1, 2005; 2(3): 113 - 121. [Abstract] [PDF]
|
|
|
|
|
|
K. A. Lindstedt and P. T. Kovanen Proteolysis of Pericellular Matrix: A Process Linking Inflammation to Plaque Destabilization and Rupture Arterioscler Thromb Vasc Biol, December 1, 2004; 24(12): 2205 - 2206. [Full Text] [PDF]
|
|
|
|
|
|
J. C. Choy, V. H.Y. Hung, A. L. Hunter, P. K. Cheung, B. Motyka, I. S. Goping, T. Sawchuk, R. C. Bleackley, T. J. Podor, B. M. McManus, et al. Granzyme B Induces Smooth Muscle Cell Apoptosis in the Absence of Perforin: Involvement of Extracellular Matrix Degradation Arterioscler Thromb Vasc Biol, December 1, 2004; 24(12): 2245 - 2250. [Abstract] [Full Text] [PDF]
|
|