Regulation of smooth muscle cell growth, function and death in vitro by activated mast cells - A potential mechanism for the weakening and rupture of atherosclerotic plaques

Biochemical Pharmacology

Volumn 66, Issue 8, 2003, Pages 1493-1498

  Leskinen, Markus J ^a   Kovanen, Petri T ^a   Lindstedt, Ken A ^a  

^a WIHURI RESEARCH INSTITUTE   (Finland)

Author keywords

Apoptosis; Atherosclerosis; Extracellular matrix; Mr; Mast cell; Matrix metalloproteinase; MMP; Molecular weight; Plaque rupture; SMC; Smooth muscle cell; TGF ; TNF ; Transforming growth factor ; Tumor necrosis factor

Indexed keywords

CHYMASE; FIBRONECTIN; INTERSTITIAL COLLAGENASE; PROTEOGLYCAN; TRANSFORMING GROWTH FACTOR BETA;

APOPTOSIS; ARTERY MUSCLE; ATHEROSCLEROTIC PLAQUE; CELL ACTIVATION; CELL ADHESION; CELL COUNT; CELL DEATH; CELL FUNCTION; CELL GROWTH; CELL SURVIVAL; COLLAGEN SYNTHESIS; CONFERENCE PAPER; CORONARY ARTERY; DISEASE COURSE; ENZYME ACTIVATION; ENZYME SYNTHESIS; EXTRACELLULAR MATRIX; HEART INFARCTION; HUMAN; MAST CELL; MITOSIS INHIBITION; NONHUMAN; PATHOGENESIS; PRIORITY JOURNAL; REGULATORY MECHANISM; SMOOTH MUSCLE FIBER; ANIMAL; ARTERIOSCLEROSIS; CELL DIVISION; INFLAMMATION; PATHOLOGY; REVIEW; RUPTURE; VASCULAR SMOOTH MUSCLE;

ANIMALS; APOPTOSIS; ARTERIOSCLEROSIS; CELL DIVISION; EXTRACELLULAR MATRIX; HUMANS; INFLAMMATION; MAST CELLS; MUSCLE, SMOOTH, VASCULAR; RUPTURE;

EID: 0642345202     PISSN: 00062952     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0006-2952(03)00503-3     Document Type: Conference Paper

References (46)

1. Stary H.C., Chandler A.B., Glagov S., Guyton J.R., Insull W. Jr., Rosenfeld M.E., Schaffer S.A., Schwartz C.J., Wagner W.D., Wissler R.W. A definition of initial, fatty streak, and intermediate lesions of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Arterioscler. Thromb. 14:1994;840-856.
2. McGill H.C. Jr. Fatty streaks in the coronary arteries and aorta. Lab. Invest. 18:1968;560-564.
3. Kovanen P.T. Atheroma formation: defective control in the intimal round-trip of cholesterol. Eur. Heart J. 11:1990;238-246.
4. Stary H.C., Chandler A.B., Dinsmore R.E., Fuster V., Glagov S., Insull W. Jr., Rosenfeld M.E., Schwartz C.J., Wagner W.D., Wissler R.W. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation. 92:1995;1355-1374.
5. Fuster V., Badimon L., Badimon J.J., Chesebro J.H. The pathogenesis of coronary artery disease and the acute coronary syndromes. N. Engl. J. Med. 326:1992;242-250.
6. Falk E. Why do plaques rupture? Circulation. 86(Suppl. III):1992;30-42.
7. Virmani R., Kolodgie F.D., Burke A.P., Farb A., Schwartz S.M. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler. Thromb. Vasc. Biol. 20:2000;1262-1275.
8. Libby P. Inflammation in atherosclerosis. Nature. 420:2002;868-874.
9. Richardson P.D., Davies M.J., Born G.V.R. Influence of plaque configuration and stress distribution on fissuring of coronary atherosclerotic plaque. Lancet. 2:1989;941-944.
10. Moreno P.R., Falk E., Palacios I.F., Newell J.B., Fuster V., Fallon J.T. Macrophage infiltration in acute coronary syndromes. Implications for plaque rupture. Circulation. 90:1994;775-778.
11. van der Wal A.C., Becker A.E., van der Loos C.M., Das P.K. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation. 89:1994;36-44.
12. Kovanen P.T., Kaartinen M., Paavonen T. Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction. Circulation. 92:1995;1084-1088.
13. Kaartinen M., Penttilä A., Kovanen P.T. Accumulation of activated mast cells in the shoulder region of human coronary atheroma, the predilection site of atheromatous rupture. Circulation. 90:1994;1669-1678.
14. Ishizaka T., Ishizaka K. Activation of mast cells for mediator release through IgE receptors. Prog. Allergy. 34:1984;188-235.
15. Sedgwick J.D., Holt P.G., Turner K.J. Production of a histamine-releasing lymphokine by antigen- or mitogen-stimulated human peripheral T cells. Clin. Exp. Immunol. 45:1981;409-418.
16. Liu M.C., Proud D., Lichtenstein L.M., MacGlashan D.W., Schleimer R.P., Adkinson N.F., Kagey-Sobotka A., Schulman E.S., Plaut M. Human lung macrophage-derived histamine-releasing activity is due to IgE-dependent factors. J. Immunol. 136:1986;2588-2595.
17. Metcalfe D.D., Kaliner M., Donlon M.A. The mast cell. Crit. Rev. Immunol. 3:1981;23-74.
18. Röhlich P., Anderson P., Uvnäs B. Electron microscope observations on compounds 48-80-induced degranulation in rat mast cells. Evidence for sequential exocytosis of storage granules. J. Cell Biol. 51:1971;465-483.
19. Kovanen P.T. The mast cell-a potential link between inflammation and cellular cholesterol deposition in atherogenesis. Eur. Heart J. 14(Suppl. K):1993;105-117.
20. Kokkonen J.O., Kovanen P.T. Stimulation of mast cells leads to cholesterol accumulation in macrophages in vitro by a mast cell granule-mediated uptake of low density lipoprotein. Proc. Natl. Acad. Sci. U.S.A. 84:1987;2287-2291.
21. Wang Y., Lindstedt K.A., Kovanen P.T. Mast cell granule remnants carry LDL into smooth muscle cells of synthetic phenotype and induce their conversion into foam cells. Arterioscler. Thromb. Vasc. Biol. 15:1995;801-810.
22. Dvorak A.M., Schleimer R.P., Schulman E.S., Lichtenstein L.M. Human mast cells use conservation and condensation mechanisms during recovery from degranulation. In vitro studies with mast cells purified from human lungs. Lab. Invest. 54:1986;663-678.
23. Laine P., Pentikäinen M.O., Wurzner R., Penttilä A., Paavonen T., Meri S., Kovanen P.T. Evidence for complement activation in ruptured coronary plaques in acute myocardial infarction. Am. J. Cardiol. 90:2002;404-408.
24. Kaartinen M., van der Wal A.C., van der Loos C.M., Piek J.J., Koch K.T., Becker A.E., Kovanen P.T. Mast cell infiltration in acute coronary syndromes: implications for plaque rupture. J. Am. Coll. Cardiol. 32:1998;606-612.
25. Wang Y., Kovanen P.T. Heparin proteoglycans released from rat serosal mast cells inhibit proliferation of rat aortic smooth muscle cells in culture. Circ. Res. 84:1999;74-83.
26. Kazi M., Lundmark K., Religa P., Gouda I., Larm O., Ray A., Swedenborg J., Hedin U. Inhibition of rat smooth muscle cell adhesion and proliferation by non-anticoagulant heparins. J. Cell Physiol. 193:2002;365-372.
27. Wang Y., Shiota N., Leskinen M.J., Lindstedt K.A., Kovanen P.T. Mast cell chymase inhibits smooth muscle cell growth and collagen expression in vitro: transforming growth factor-beta1-dependent and -independent effects. Arterioscler. Thromb. Vasc. Biol. 21:2001;1928-1933.
28. Kaartinen M., Penttilä A., Kovanen P.T. Mast cells in rupture-prone areas of human coronary atheromas produce and store TNF-α Circulation. 94:1996;2787-2792.
29. Saren P., Welgus H.G., Kovanen P.T. TNF-alpha and IL-1beta selectively induce expression of 92-kDa gelatinase by human macrophages. J. Immunol. 157:1996;4159-4165.
30. Baram D., Vaday G.G., Salamon P., Drucker I., Hershkoviz R., Mekori Y.A. Human mast cells release metalloproteinase-9 on contact with activated T cells: juxtacrine regulation by TNF-alpha. J. Immunol. 167:2001;4008-4016.
31. Di Girolamo N., Wakefield D. In vitro and in vivo expression of interstitial collagenase/MMP-1 by human mast cells. Dev. Immunol. 7:2000;131-142.
32. Nikkari S.T., O'Brien K.D., Ferguson M., Hatsukami T., Welgus H.G., Alpers C.E., Clowes A.W. Interstitial collagenase (MMP-1) expression in human carotid atherosclerosis. Circulation. 92:1995;1393-1398.
33. Vartio T., Seppä H., Vaheri A. Susceptibility of soluble and matrix fibronectins to degradation by tissue proteinases, mast cells chymase and cathepsin G. J. Biol. Chem. 256:1981;471-477.
34. Lohi J., Harvima I., Keski-Oja J. Pericellular substrates of human mast cell tryptase: 72,000 dalton gelatinase and fibronectin. J. Cell Biochem. 50:1992;337-349.
35. Birkedal-Hansen H., Moore W.G., Bodden M.K., Windsor L.J., Birkedal-Hansen B., DeCarlo A., Engler J.A. Matrix metalloproteinases: a review. Crit. Rev. Oral Biol. Med. 4:1993;197-250.
36. 84 bond by mast cell chymase. J. Biol. Chem. 269:1994;18134-18140.
37. Gruber B.L., Marchese M.J., Suzuki K., Schwartz L.B., Okada Y., Nagase H., Ramamurthy N.S. Synovial procollagenase activation by human mast cell tryptase dependence upon matrix metalloproteinase 3 activation. J. Clin. Invest. 84:1989;1657-1662.
38. Libby P. Molecular bases of the acute coronary syndromes. Circulation. 91:1995;2844-2850.
39. Lätti S., Leskinen M.J., Wang Y., Kovanen P.T., Lindstedt K.A. Mast cell-mediated apoptosis of endothelial cells in vitro: a paracrine mechanism involving TNF-alpha-mediated down-regulation of bcl-2 expression. J. Cell Physiol. 195:2003;130-138.
40. Wallach D. Cell death induction by TNF: a matter of self control. Trends Biochem. Sci. 22:1997;107-109.
41. Hara M., Matsumori A., Ono K., Kido H., Hwang M.W., Miyamoto T., Iwasaki A., Okada M., Nakatani K., Sasayama S. Mast cells cause apoptosis of cardiomyocytes and proliferation of other intramyocardial cells in vitro. Circulation. 100:1999;1443-1449.
42. Leskinen M., Wang Y., Leszczynski D., Lindstedt K.A., Kovanen P.T. Mast cell chymase induces apoptosis of vascular smooth muscle cells. Arterioscler. Thromb. Vasc. Biol. 21:2001;516-522.
43. Leskinen M.J., Lindstedt K.A., Wang Y., Kovanen P.T. Mast cell chymase induces smooth muscle cell apoptosis by a mechanism involving fibronectin degradation and disruption of focal adhesions. Arterioscler. Thromb. Vasc. Biol. 23:2003;238-243.
44. Tchougounova E., Forsberg E., Angelborg G., Kjellen L., Pejler G. Altered processing of fibronectin in mice lacking heparin. A role for heparin-dependent mast cell chymase in fibronectin degradation. J. Biol. Chem. 276:2001;3772-3777.
45. Lindstedt L., Lee M., Kovanen P.T. Chymase bound to heparin is resistant to its natural inhibitors and capable of proteolyzing high density lipoproteins in aortic intimal fluid. Atherosclerosis. 155:2001;87-97.
46. Karsan A., Yee E., Harlan J.M. Endothelial cell death induced by tumor necrosis factor-alpha is inhibited by the Bcl-2 family member, A1. J. Biol. Chem. 271:1996;27201-27204.