In: Circulation, 2007, vol. 115, p. 2188-2195
Background— The circadian clock regulates biological processes including cardiovascular function and metabolism. In the present study, we investigated the role of the circadian clock gene Period2 (Per2) in endothelial function in a mouse model. Methods and Results— Compared with the wild-type littermates, mice with Per2 mutation exhibited impaired...
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In: Current Hypertension Reports, 2006, vol. 8, no. 1, p. 54-59
Decreased endothelial nitric oxide (NO) bioavailability as it relates to endothelial dysfunction plays an important role in various cardiovascular disorders, including atheroÂsclerosis. Recent research has provided evidence that endothelial dysfunction in atherosclerosis is not primarily caused by decreased endothelial NO synthase (eNOS) gene expression, but rather deregulation of eNOS...
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In: Journal of Vascular Research, 2006, vol. 43, no. 4, p. 338-346
The remarkable patency of internal mammary artery (MA) grafts compared to saphenous vein (SV) grafts has been related to different biological properties of the two blood vessels. We examined whether proliferation and apoptosis of vascular smooth muscle cells (VSMC) from human coronary artery bypass vessels differ according to patency rates. Methods and Results: Proliferation rates to serum...
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In: Circulation, 2006, vol. 114, no. 14, p. 1512-1521
Background— Subacute stent thrombosis is a major clinical concern, and the search for new molecules to cover stents remains important. Dimethyl sulfoxide (DMSO) is used for preservation of hematopoietic progenitor cells and is infused into patients undergoing bone marrow transplantation. Despite its intravenous application, the impact of DMSO on vascular cells has not been assessed....
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In: Cardiovascular Research, 2005, vol. 68, no. 3, p. 475-482
Objective: Pulsatile forces regulate vascular remodeling and trigger vascular diseases such as saphenous vein graft disease. The saphenous vein is exposed to high pressure and pulsatility only after implantation. Statins have been proved to reduce the incidence of vein graft failure. Thus, we investigated the molecular mechanisms of pulsatile stretch-induced saphenous vein smooth...
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In: American Journal of Physiology - Heart & Circulatory Physiology, 2005, vol. 289, p. H1807-H1813
Adipocytes and perivascular adipose tissue are emerging as regulators of vascular function. The effects of adipocytes and perivascular adipose tissue on human smooth muscle cell (SMC) proliferation were investigated. Conditioned medium was prepared from cultured premature and differentiated 3T3-L1 adipocytes and from periaortic adipose tissue from young (3 mo) and old (24 mo) Wistar-Kyoto (WKY)...
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In: Basic Research in Cardiology, 2005, vol. 100(2), p. 102
Nitric oxide (NO) and monocyte chemoattractant protein–1 (MCP-1) exert partly opposing effects in vascular biology. NO plays pleiotropic vasoprotective roles including vasodilation and inhibition of platelet aggregation, smooth muscle cell proliferation, and endothelial monocyte adhesion, the last effect being mediated by MCP–1 downregulation. Early stages of arteriosclerosis are associated...
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In: Journal of Thoracic and Cardiovascular Surgery, 2004, vol. 127, no. 1, p. 20-26
Background Bypass graft disease is related to proliferation and migration of vascular smooth muscle cells and to platelet activation with thrombus formation. Nitric oxide inhibits these biological responses; it has never been demonstrated, however, whether this occurs in intact human vascular tissue after endothelial nitric oxide synthase gene transfer. Methods We examined whether endothelial...
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In: International Journal of Obesity, 2004, vol. 28, p. S58-65
In humans and most animal models, the development of obesity leads not only to increased fat depots in classical adipose tissue locations but also to significant lipid deposits within and around other tissues and organs, a phenomenon known as ectopic fat storage. The purpose of this review is to explore the possible locations of ectopic fat in key target-organs of cardiovascular control (heart,...
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In: Circulation, 2004, vol. 110, p. 3708-3714
Background— Arginase competes with endothelial nitric oxide synthase (eNOS) for the substrate L-arginine and decreases NO production. This study investigated regulatory mechanisms of arginase activity in endothelial cells and its role in atherosclerosis. Methods and Results— In human endothelial cells isolated from umbilical veins, thrombin concentration- and time-dependently stimulated...
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