[Seite 23↓]


[1] Lusis, A. J. (2000): Atherosclerosis, Nature, (vol. 407), No. 6801, pp.233-41..

[2] Libby, P.; Ridker, P.M. and Maseri, A. (2002): Inflammation and atherosclerosis, Circulation, (vol. 105), pp.1135-43.

[3] Ross, R. (1999): Atherosclerosis - an inflammatory disease, N Engl J Med, (vol. 340), pp.115-26.

[4] Raines, E. W. and Ross, R. (1993): Smooth muscle cells and the pathogenesis of the lesions of atherosclerosis, Br Heart J, (vol. 69), No. 1 Suppl, pp.S30-7.

[5] Ross, R. (1993): The pathogenesis of atherosclerosis: a perspective for the 1990s, Nature, (vol. 362), No. 6423, pp.801-9.

[6] Goetze, S.; Xi, X-P.; Graf, K.; Fleck, E.; Hsueh, W.A. and Law, R.E. (1999): Troglitazone inhibits AII-induced ERK 1/2 nuclear translocation and activation in vascular smooth muscle cells, FEBS Lett, (vol. 452), pp.277-82.

[7] Goetze, S.; Kintscher, U.; Kaneshiro, K.; Meehan, W. P.; Collins, A.; Fleck, E.; Hsueh, W. A. and Law, R. E. (2001): TNFalpha induces expression of transcription factors c-fos, Egr-1, and Ets-1 in vascular lesions through extracellular signal-regulated kinases 1/2, Atherosclerosis, (vol. 159), No. 1, pp.93-101..

[8] Goetze, S.; Kintscher, U.; Kim, S.; Meehan, W.P.; Kaneshiro, K.; Collins, A.R.; Fleck, E.; Hsueh, W.A. and Law, R.E. (2001): PPARgamma-ligands inhibit nuclear but not cytosolic ERK-MAPK-regulated steps in vascular smooth muscle cell migration., J Cardiovasc Pharmacol, (vol. 38), pp.909-921.

[9] Barbier, O.; Torra, I.P.; Duguay, Y.; Blanquart, C.; Fruchart, J.C.; Glineur, C. and Staels, B. (2002): Pleiotropic actions of peroxisome proliferator-activated receptors in lipid metabolism and atherosclerosis., Arterioscl Thromb Vasc Biol, (vol. 22), pp.717-26.

[10] Hsueh, W.A. and Law, R.E: (2001): PPARgamma and atherosclerosis: effects on cell growth and movement, Arterioscler Thromb Vasc Biol, (vol. 21), pp.1891-5.

[11] Neve, B. P.; Fruchart, J. and Staels, B. (2000): Role of the peroxisome proliferator-activated receptors (PPAR) in atherosclerosis, Biochem Pharmacol, (vol. 60), No. 8, pp.1245-50.

[12] Bishop-Bailey, D. (2000): Peroxisome proliferator-activated receptors in the cardiovascular system, Br J Pharmacol, (vol. 129), No. 5, pp.823-34.

[13] Goetze, S.; Xi, X. P.; Kawano, H.; Gotlibowski, T.; Fleck, E.; Hsueh, W. A. and Law, R. E. (1999): PPAR gamma-ligands inhibit migration mediated by multiple chemoattractants in vascular smooth muscle cells, J Cardiovasc Pharmacol, (vol. 33), No. 5, pp.798-806.

[14] Goetze, S.; Kim, S. ; Xi, X.P.; Graf, K.; Yang, D.C:; Fleck, E.; Meehan, P.W.; Hsueh, W.A. and Law, R.E. (2000): Troglitazone inhibits mitogenic signaling by insulin in vascular smooth muscle cells, J Cardiovasc Pharmacol, (vol. 35), pp.749-57.

[15] Law, R. E.; Goetze, S.; Xi, X. P.; Jackson, S.; Kawano, Y.; Demer, L.; Fishbein, M. C.; Meehan, W. P. and Hsueh, W. A. (2000): Expression and function of PPARgamma in rat and human vascular smooth muscle cells, Circulation, (vol. 101), No. 11, pp.1311-8.

[16] Goetze, S.; Bungenstock, A.; Eilers, F.; Czupalla, C.; Stawowy, P; Kintscher, U.; Spencer-Hänsch, C.; Nürnberg, B.; Graf, K.; Law, R.E.; Fleck, E. and Gräfe, M (2002): Leptin-induced migration of endothelial cells is Akt- and MAPK-dependent and inhibited by PPARgamma-ligands, Hypertension, (vol. 40), pp.748-754.

[17] Goetze, S.; Eilers, F.; Bungenstock, A.; Kintscher, U.; Stawowy, P.; Blaschke, F.; Graf, K.; Law, R.E:; Fleck, E. and Gräfe, M. (2002): PPAR-activators inhibit endothelial cell migration by targeting Akt, Biochem Biophys Res Comm, (vol. 293), pp.1431-7.

[Seite 24↓]

[18] Marx, N.; Schonbeck, U.; Lazar, M. A.; Libby, P. and Plutzky, J. (1998): Peroxisome proliferator-activated receptor gamma activators inhibit gene expression and migration in human vascular smooth muscle cells, Circ Res, (vol. 83), No. 11, pp.1097-103. http://www.circresaha.org/cgi/content/full/83/11/1097

[19] Marx, N.; Sukhova, G.; Murphy, C.; Libby, P. and Plutzky, J. (1998): Macrophages in human atheroma contain PPARgamma: differentiation- dependent peroxisomal proliferator-activated receptor gamma(PPARgamma) expression and reduction of MMP-9 activity through PPARgamma activation in mononuclear phagocytes in vitro, Am J Pathol, (vol. 153), No. 1, pp.17-23.

[20] Marx, N.; Bourcier, T.; Sukhova, G. K.; Libby, P. and Plutzky, J. (1999): PPARgamma activation in human endothelial cells increases plasminogen activator inhibitor type-1 expression: PPARgamma as a potential mediator in vascular disease, Arterioscler Thromb Vasc Biol, (vol. 19), No. 3, pp.546-51. http://www.atvbaha.org/cgi/content/full/19/3/546

[21] Bishop-Bailey, D. and Hla, T. (1999): Endothelial cell apoptosis induced by the peroxisome proliferator-activated receptor (PPAR) ligand 15-deoxy-Delta12, 14-prostaglandin J2, J Biol Chem, (vol. 274), No. 24, pp.17042-8. http://www.jbc.org/cgi/content/full/274/24/17042

[22] Staels, B.; Koenig, W.; Habib, A.; Merval, R.; Lebret, M.; Torra, I. P.; Delerive, P.; Fadel, A.; Chinetti, G.; Fruchart, J. C.; Najib, J.; Maclouf, J. and Tedgui, A. (1998): Activation of human aortic smooth-muscle cells is inhibited by PPARalpha but not by PPARgamma activators, Nature, (vol. 393), No. 6687, pp.790-3.

[23] Kliewer, S.A.; Sundseth, S.S:; Jones, S.A.; Brown, P.J.; Wisely, G.B.; Koble, C.S.; Devchand, P.; Wahli, W.; Willson, T.M.; Lenhard, J.M. and Lehmann, J.M. (1997): Fatty acids and eisosanoids regulate gene expression through direct interactions with peroxisome proliferator-activated receptor alpha and gamma., Proc Natl Acad Sci, (vol. 94), pp.4318-23.

[24] Forman, B.M.; Chen, J. and Evans, R.M. (1997): Hypolipidemic drugs, polyunsaturated fatty acids, and eicosanoids are ligands for peroxisome proliferator-activated receptors alpha and delta., Proc Natl Acad Sci, (vol. 94), pp.4312-17.

[25] Kliewer, S. A.; Lenhard, J. M.; Willson, T. M.; Patel, I.; Morris, D. C. and Lehmann, J. M. (1995): A prostaglandin J2 metabolite binds peroxisome proliferator-activated receptor gamma and promotes adipocyte differentiation, Cell, (vol. 83), No. 5, pp.813-9.

[26] Nagy, Laszlo; Tontonoz, Peter; Alvarez, Jacqueline G. A.; Chen, Hongwu and Evans, Ronald M. (1998): Oxidized LDL Regulates Macrophage Gene Expression through Ligand Activation of PPARg, Cell, (vol. 93), No. April 17, pp.229-240.

[27] Lehmann, J. M.; Moore, L. B.; Smith-Oliver, T. A.; Wilkison, W. O.; Willson, T. M. and Kliewer, S. A. (1995): An antidiabetic thiazolidinedione is a high affinity ligand for peroxisome proliferator-activated receptor gamma (PPAR gamma), J Biol Chem, (vol. 270), No. 22, pp.12953-6. http://www.ncbi.nlm.nih.gov/cgi-bin/Entrez/referer? , http://www.ncbi.nlm.nih.gov/htbin-post/Omim/getmim%3ffield=medline_uid&search=7768881

[28] Schoonjans, K.; Peinado-Onsurbe, J.; Lefebvre, A.M.; Heyman, R.A.; Briggs, M.; Deeb, S.; Staels, B. and Auwerx, J. (1996): PPARalpha and gamma activators direct a distinct tissue-specific transcriptional response via a PPRE in the lipoprotein lipase gene., EMBO J, (vol. 15), pp.5336-48.

[29] Marx, N. and Hombach, V. (2001): Peroxisome proliferator-activated receptors (PPARs) in the vessel wall: new regulators of gene expression in vascular cells, Z Kardiol, (vol. 90(7)), pp.470-7.

[30] Law, R. E.; Meehan, W. P.; Xi, X. P.; Graf, K.; Wuthrich, D. A.; Coats, W.; Faxon, D. and Hsueh, W. A. (1996): Troglitazone inhibits vascular smooth muscle cell growth and intimal hyperplasia, J Clin Invest, (vol. 98), No. 8, pp.1897-905. http://www.ncbi.nlm.nih.gov/cgi-bin/Entrez/referer?, http://www.jci.org/cgi/content/full/98/8/1897

[31] Goetze, S.; Xi, X. P.; Kawano, Y.; Kawano, H.; Fleck, E.; Hsueh, W. A. and Law, R. E. (1999): TNF-alpha-induced migration of vascular smooth muscle cells is MAPK dependent, Hypertension, (vol. 33), No. 1 Pt 2, pp.183-9. http://www.hypertensionaha.org/cgi/content/full/33/1/183

[32] Kintscher, U.; Goetze, S.; Wakino, S.; Kim, S.; Nagpal, S.; Chandraratna, R. A.; Graf, K.; Fleck, E.; Hsueh, W. A. and Law, R. E. (2000): Peroxisome proliferator-activated receptor and retinoid X receptor ligands inhibit monocyte chemotactic protein-1-directed migration of monocytes, Eur J Pharmacol, (vol. 401), No. 3, pp.259-70..

[Seite 25↓]

[33] Nigro, J.; Dilley, R.J. and Little, P.J. (2002): Differential effects of gemfibrozil on migration, proliferation and proteoglycan production in human vascular smooth muscle cells., Atherosclerosis, (vol. 162), pp.119-29.

[34] Schwartz, S. M. (1997): Perspectives series: cell adhesion in vascular biology. Smooth muscle migration in atherosclerosis and restenosis, J Clin Invest, (vol. 99), No. 12, pp.2814-6. http://www.ncbi.nlm.nih.gov/cgi-bin/Entrez/referer?, http://www.jci.org/cgi/content/full/99/12/2814

[35] Casscells, W. (1992): Migration of smooth muscle and endothelial cells. Critical events in restenosis, Circulation, (vol. 86), No. 3, pp.723-9.

[36] Graf, K.; Xi, X. P.; Yang, D.; Fleck, E.; Hsueh, W. A. and Law, R. E. (1997): Mitogen-activated protein kinase activation is involved in platelet- derived growth factor-directed migration by vascular smooth muscle cells, Hypertension, (vol. 29), No. 1 Pt 2, pp.334-9.

[37] Nelson, P. R.; Yamamura, S.; Mureebe, L.; Itoh, H. and Kent, K. C. (1998): Smooth muscle cell migration and proliferation are mediated by distinct phases of activation of the intracellular messenger mitogen-activated protein kinase, J Vasc Surg, (vol. 27), No. 1, pp.117-25.

[38] Xi, X-P.; Graf, K.; Goetze, S.; Fleck, E.; Hsueh, W.A. and Law, R.E. (1999): Central Role of the MAPK pathway in AII-mediated DNA-synthesis and migration in rat vascular smooth muscle cells, Arteriosclerosis, Thrombosis and Vascular Biology, (vol. 19), pp.73-82.

[39] Klemke, R. L.; Cai, S.; Giannini, A. L.; Gallagher, P. J.; de Lanerolle, P. and Cheresh, D. A. (1997): Regulation of cell motility by mitogen-activated protein kinase, J Cell Biol, (vol. 137), No. 2, pp.481-92. http://www.ncbi.nlm.nih.gov/cgi-bin/Entrez/referer?, http://www.jcb.org/cgi/content/full/137/2/481

[40] Gille, H.; Kortenjann, M.; Thomae, O.; Moomaw, C.; Slaughter, C.; Cobb, M. H. and Shaw, P. E. (1995): ERK phosphorylation potentiates Elk-1-mediated ternary complex formation and transactivation, Embo J, (vol. 14), No. 5, pp.951-62.

[41] Gille, H.; Kortenjann, M.; Strahl, T. and Shaw, P. E. (1996): Phosphorylation-dependent formation of a quaternary complex at the c- fos SRE, Mol Cell Biol, (vol. 16), No. 3, pp.1094-102.

[42] Cheresh, D. A.; Leng, J. and Klemke, R. L. (1999): Regulation of cell contraction and membrane ruffling by distinct signals in migratory cells, J Cell Biol, (vol. 146), No. 5, pp.1107-16.

[43] Pauly, R. R.; Passaniti, A.; Bilato, C.; Monticone, R.; Cheng, L.; Papadopoulos, N.; Gluzband, Y. A.; Smith, L.; Weinstein, C.; Lakatta, E. G. and et al. (1994): Migration of cultured vascular smooth muscle cells through a basement membrane barrier requires type IV collagenase activity and is inhibited by cellular differentiation, Circ Res, (vol. 75), No. 1, pp.41-54.

[44] Zempo, N.; Koyama, N.; Kenagy, R. D.; Lea, H. J. and Clowes, A. W. (1996): Regulation of vascular smooth muscle cell migration and proliferation in vitro and in injured rat arteries by a synthetic matrix metalloproteinase inhibitor, Arterioscler Thromb Vasc Biol, (vol. 16), No. 1, pp.28-33.

[45] Haas, T.L.; Stitelmann, D.; Davis, S.J.; Apte, S.S. and Madri, J.A. (1999): Egr-1 mediates extracellular matrix-driven transcription of membrane type I matrix metalloproteinase in endothelium., J Biol Chem, (vol. 274), pp.22679-685.

[46] Westermarck, J. and Kahari, V.M. (1999): Regulation of matrix metalloproteinase expression in tumor invasion, FASEB J, (vol. 13), pp.781-792.

[47] Santiago, F.S.; Atkins, D.G. and Kachigian, L.M. (1999): Vascular smooth muscle cell proliferation and regrowth after mechanical injury in vitro are Egr-1/NGFI-A-dependent, Am J Pathol, (vol. 155), pp.897-905.

[Seite 26↓]

[48] Iwasaka, I.; Tanaka, K.; Abe, M. and Sato, Y. (1996): Ets-1 regulates angiogenesis by inducing the expression of urokinase-type plasminogen activator and matrix metalloproteinase-1 and the migration of vascualr endothelial cells, J Cell Physiol, (vol. 169), pp.522-531.

[49] Dimmeler, S.; Dernbach, E. and Zeiher, A. M. (2000): Phosphorylation of the endothelial nitric oxide synthase at ser-1177 is required for VEGF-induced endothelial cell migration, FEBS Lett, (vol. 477), No. 3, pp.258-62.

[50] Duan, C.; Bauchat, J. R. and Hsieh, T. (2000): Phosphatidylinositol 3-kinase is required for insulin-like growth factor-I-induced vascular smooth muscle cell proliferation and migration, Circ Res, (vol. 86), No. 1, pp.15-23..

[51] Imai, Y. and Clemmons, D. R. (1999): Roles of phosphatidylinositol 3-kinase and mitogen-activated protein kinase pathways in stimulation of vascular smooth muscle cell migration and deoxyriboncleic acid synthesis by insulin-like growth factor-I, Endocrinology, (vol. 140), No. 9, pp.4228-35..

[52] Ricote, M.; Li, A. C.; Willson, T. M.; Kelly, C. J. and Glass, C. K. (1998): The peroxisome proliferator-activated receptor-gamma is a negative regulator of macrophage activation, Nature, (vol. 391), No. 6662, pp.79-82.

[53] Fukuda, M.; Gotoh, Y. and Nishida, E. (1997): Interaction of MAP kinase with MAP kinase kinase: its possible role in the control of nucleocytoplasmic transport of MAP kinase, Embo J, (vol. 16), No. 8, pp.1901-8. http://www.ncbi.nlm.nih.gov/cgi-bin/Entrez/referer?, http://www.emboj.org/cgi/content/full/16/8/1901

[54] Liao, D. F.; Monia, B.; Dean, N. and Berk, B. C. (1997): Protein kinase C-zeta mediates angiotensin II activation of ERK1/2 in vascular smooth muscle cells, J Biol Chem, (vol. 272), No. 10, pp.6146-50. http://www.ncbi.nlm.nih.gov/cgi-bin/Entrez/referer?, http://www.jbc.org/cgi/content/full/272/10/6146

[55] Oda, N.; Abe, M. and Sato, Y. (1999): ETS-1 converts endothelial cells to the angiogenic phenotype by inducing the expression of matrix metalloproteinases and integrin beta3, J Cell Physiol, (vol. 178), No. 2, pp.121-32.

[56] Patel, L.; Pass, I.; Coxon, P.; Downes, C.P.; Smith, S.A. and Macphee, C.H. (2001): Tumor suppressor and anti-inflammatory actions of PPARgamma agonists are mediated via upregulation of PTEN, Curr Biol, (vol. 11), pp.764-8.

[57] Arico, S.; Petiot, A.; Bauvy, C.; Dubbelhuis, P.F.; Meijer, A.J.; Codogno, P. and Ogier-Denis, E. (2001): The tumor suppressor PTEN positively regulates macroautophagy by inhibiting the PI3 Kinase / PKB pathway, J Biol Chem, (vol. 276), pp.35243-6.

[58] Goetze, S.; Kintscher, U.; Kawano, H.; Kawano, Y.; Wakino, S.; Fleck, E.; Hsueh, W. A. and Law, R. E. (2000): Tumor necrosis factor alpha inhibits insulin-induced mitogenic signaling in vascular smooth muscle cells, J Biol Chem, (vol. 275), No. 24, pp.18279-83.

[59] Xi, X. P.; Graf, K.; Goetze, S.; Hsueh, W. A. and Law, R. E. (1997): Inhibition of MAP kinase blocks insulin-mediated DNA synthesis and transcriptional activation of c-fos by Elk-1 in vascular smooth muscle cells, FEBS Lett, (vol. 417), No. 3, pp.283-6.

[60] Saltiel, A. R. (1996): Diverse signaling pathways in the cellular actions of insulin, Am J Physiol, (vol. 270), No. 3 Pt 1, pp.E375-85.

[61] Wasylyk, B.; Hagman, J. and Hartmann, A.G. (1998): Ets transcription factors: nuclear effectors of the Ras-MAP-Kinase signaling pathway, Trends Biochem Sci, (vol. 23), pp.213-216.

[62] Collins, A. R.; Meehan, W. P.; Kintscher, U.; Jackson, S.; Wakino, S.; Noh, G.; Palinski, W.; Hsueh, W. A. and Law, R. E. (2001): Troglitazone inhibits formation of early atherosclerotic lesions in diabetic and nondiabetic low density lipoprotein receptor-deficient mice, Arterioscler Thromb Vasc Biol, (vol. 21), No. 3, pp.365-71..

[63] Minamikawa, J.; Tanaka, S.; Yamauchi, M.; Inoue, D. and Koshiyama, H. (1998): Potent inhibitory effect of troglitazone on carotid artery wall thickness in type 2 diabetes., J Clin Endocrinol Metab, (vol. 83), pp.1818-20.

[Seite 27↓]

[64] Koshiyama, H.; Shimono, D.; Kuwamura, N.; Minamikawa, J. and Nakamura, Y. (2001): Inhibitory effect of pioglitazone on carotid artery wall thickness in type 2 diabetes., J Clin Endocrinol Metab, (vol. 86), pp.3452-6.

[65] Zuckerman, S.H.; Kauffman, R.F. and Evans, G.F. (2002): Peroxisome proliferator-activated receptor alpha, gamma coagonist LY465608 inhibits macrophage activation and atherosclerosis in apolipoprotein E knockout mice., Lipids, (vol. 37), pp.487-94.

[66] Hahmann, H.W.; Bunte, T.; Hellwig, N.; Hau, U.; Becker, D.; Dyckmans, J.; Keller, H.E. and Schieffer, H.J. (1991): Progression and regression of minor coronary arterial narrowings by quantitative angiography after fenofibrate therapy., Am J Cardiol, (vol. 67), pp.957-61.

[67] Steiner, G.; Stewart, D. and Hosking, J.D. (1999): Baseline characteristics of the study population in the diabetes atherosclerosis intervention study (DAIS). World health organization collaborating centre for the study of atherosclerosis in diabetes., Am J Cardiol, (vol. 84), pp.1004-10.

[68] de Faire, U.; Ericsson, C.G.; Grip, L.; Nilsson, J.; Svane, B. and Hamsten, A. (1997): Retardation of coronary atherosclerosis: the bezafibrate coronary atherosclerosis intervention trial (BECAIT) and other angiographic trials., Cardiovasc Drugs Ther, (vol. 11 (Suppl 1)), pp.257-63.

[69] Rubins, H.B.; Robins, S.J.; Collins, D.; Fye, C.L.; Anderson, J.W.; Elam, M.B.; Faas, F.H.; Linares, E.; Schaefer, E.J.; Schectman, G.; Wilt, T.J. and Wittes, J. (1999): Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. Veterans affairs high-density lipoprotein cholesterol intervention trial study group., N Engl J Med, (vol. 341), pp.410-8.

[70] Group, DAIS Study (2001): Effect of fenofibrate on progression of coronary-artery disease in type 2 diabetes: the Diabetes atherosclerosis intervention study, a randomized study., Lancet, (vol. 357), pp.905-10.

[71] Frick, M.H.; Syvänne, M.; Nieminen, M.S.; Kauma, H.; Majahalme, S.; Virtanen, V.; Kesäniemi, Y.A.; Pasternack, A. and Taskinen, M.R. (1997): Prevention of the angiographic progression of coronary and vein-graft atherosclerosis by gemfibrozil after coronary bypass surgery in men with low levels of HDL cholesterol., Circulation, (vol. 96), pp.2137-43.

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