Orally administered penicillamine is a potent inhibitor of neointimal and medial thickening in porcine saphenous vein-carotid artery interposition grafts.
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G. Angelini | Jason L Johnson | A. Yim | Jason L. Johnson | S. Wan | J. Jeremy | N. Shukla
[1] R. Ian Freshney,et al. Culture of Animal Cells: A Manual of Basic Technique and Specialized Applications , 2010 .
[2] A. Mandinova,et al. Inhibition of in-stent restenosis by oral copper chelation in porcine coronary arteries. , 2006, American journal of physiology. Heart and circulatory physiology.
[3] G. Angelini,et al. Does oxidative stress change ceruloplasmin from a protective to a vasculopathic factor? , 2006, Atherosclerosis.
[4] G. Angelini,et al. Penicillamine administration reverses the inhibitory effect of hyperhomocysteinaemia on endothelium-dependent relaxation and superoxide formation in the aorta of the rabbit. , 2006, European journal of pharmacology.
[5] G. Angelini,et al. Calcium and the replication of human vascular smooth muscle cells: studies on the activation and translocation of extracellular signal regulated kinase (ERK) and cyclin D1 expression. , 2005, European journal of pharmacology.
[6] G. Angelini,et al. Reactive oxygen species, vascular disease and cardiovascular surgery. , 2004, Current vascular pharmacology.
[7] G. Angelini,et al. The endothelin 1A receptor antagonist BSF 302146 is a potent inhibitor of neointimal and medial thickening in porcine saphenous vein-carotid artery interposition grafts. , 2004, The Journal of thoracic and cardiovascular surgery.
[8] Yung-Hyun Choi,et al. PDTC, metal chelating compound, induces G1 phase cell cycle arrest in vascular smooth muscle cells through inducing p21Cip1 expression: Involvement of p38 mitogen activated protein kinase , 2004, Journal of cellular physiology.
[9] Richard W. Martin,et al. High-dose versus low-dose D-penicillamine in early diffuse systemic sclerosis trial: lessons learned. , 2004, Seminars in arthritis and rheumatism.
[10] S. Merajver,et al. Tetrathiomolybdate inhibits angiogenesis and metastasis through suppression of the NFkappaB signaling cascade. , 2003, Molecular cancer research : MCR.
[11] R. Soldi,et al. Copper chelation represses the vascular response to injury , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[12] G. Brewer. Tetrathiomolybdate anticopper therapy for Wilson's disease inhibits angiogenesis, fibrosis and inflammation , 2003, Journal of cellular and molecular medicine.
[13] G. Angelini,et al. Sustained increases of plasma homocysteine, copper, and serum ceruloplasmin after coronary artery bypass grafting. , 2002, The Annals of thoracic surgery.
[14] V. Culotta,et al. Copper Chaperones: Personal Escorts for Metal Ions , 2002, Journal of bioenergetics and biomembranes.
[15] M. Won,et al. Oxidative modification of human ceruloplasmin by peroxyl radicals. , 2001, Biochimica et biophysica acta.
[16] M. Burkitt. A critical overview of the chemistry of copper-dependent low density lipoprotein oxidation: roles of lipid hydroperoxides, alpha-tocopherol, thiols, and ceruloplasmin. , 2001, Archives of biochemistry and biophysics.
[17] G. Angelini,et al. Oxidative Stress, Nitric Oxide, and Vascular Disease , 2001, Journal of cardiac surgery.
[18] L. Campeau. Lipid lowering and coronary bypass graft surgery , 2000, Current opinion in cardiology.
[19] B. Mazumder,et al. Ceruloplasmin and cardiovascular disease. , 2000, Free radical biology & medicine.
[20] S. Choi,et al. Fragmentation of human ceruloplasmin induced by hydrogen peroxide. , 2000, Biochimie.
[21] D. McMillin,et al. On the lability and functional significance of the type 1 copper pool in ceruloplasmin , 1999, JBIC Journal of Biological Inorganic Chemistry.
[22] H. Daida,et al. [Elevated levels of plasma homocysteine related to saphenous vein graft disease after coronary artery bypass graft surgery]. , 1998, Journal of cardiology.
[23] A. Mitchell,et al. Copper, lysyl oxidase, and extracellular matrix protein cross-linking. , 1998, The American journal of clinical nutrition.
[24] R. Favaloro,et al. Critical analysis of coronary artery bypass graft surgery: a 30-year journey. , 1998, Journal of the American College of Cardiology.
[25] E J Topol,et al. Aortocoronary saphenous vein graft disease: pathogenesis, predisposition, and prevention. , 1998, Circulation.
[26] B. Hultberg,et al. The cell-damaging effects of low amounts of homocysteine and copper ions in human cell line cultures are caused by oxidative stress. , 1997, Toxicology.
[27] G. Breithardt,et al. Copper-induced inflammatory reactions of rat carotid arteries mimic restenosis/arteriosclerosis-like neointima formation. , 1997, Atherosclerosis.
[28] Y. Wilson,et al. Hyperhomocysteinaemia is a risk factor for vein graft stenosis. , 1996, European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery.
[29] W J Keon,et al. Coronary bypass graft fate and patient outcome: angiographic follow-up of 5,065 grafts related to survival and reoperation in 1,388 patients during 25 years. , 1996, Journal of the American College of Cardiology.
[30] T. Ogihara,et al. Plasma Copper and Antioxidant Status in Wilson's Disease , 1995, Pediatric Research.
[31] M. Davies,et al. Pathobiology of intimal hyperplasia , 1994, The British journal of surgery.
[32] B. Portmann,et al. Value of urinary copper excretion after penicillamine challenge in the diagnosis of Wilson's disease , 1992, Hepatology.
[33] A. Newby,et al. Dual role of matrix metalloproteinases (matrixins) in intimal thickening and atherosclerotic plaque rupture. , 2005, Physiological reviews.
[34] G. Angelini,et al. Oxidant stress, nitric oxide and vascular disease , 2002 .
[35] F. Castellino,et al. Remodeling of the vessel wall after copper-induced injury is highly attenuated in mice with a total deficiency of plasminogen activator inhibitor-1. , 2001, The American journal of pathology.
[36] G. Angelini,et al. The endothelin(A) (ETA) receptor antagonist, BSF 302146, is a potent inhibitor of porcine vein graft thickening, in vivo , 2000 .