farnesyl-pyrophosphate and Arteriosclerosis

farnesyl-pyrophosphate has been researched along with Arteriosclerosis* in 2 studies

Other Studies

2 other study(ies) available for farnesyl-pyrophosphate and Arteriosclerosis

Article	Year
Cerivastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme a reductase, inhibits endothelial cell proliferation induced by angiogenic factors in vitro and angiogenesis in in vivo models. Arteriosclerosis, thrombosis, and vascular biology, 2002, Apr-01, Volume: 22, Issue:4 Cerivastatin is an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase. It inhibits the biosynthesis of cholesterol and its precursors: farnesyl pyrophosphate and geranylgeranyl pyrophosphate (GGPP), which are involved in Ras and RhoA cell signaling, respectively. Statins induce greater protection against vascular risk than that expected by cholesterol reduction. Therefore, cerivastatin could protect plaque against rupture, an important cause of ischemic events. In this study, the effect of cerivastatin was tested on angiogenesis because it participates in plaque progression and plaque destabilization. Cerivastatin inhibits in vitro the microvascular endothelial cell proliferation induced by growth factors, whereas it has no effect on unstimulated cells. This growth arrest occurs at the G(1)/S phase and is related to the increase of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1). These effects are reversed by GGPP, suggesting that the inhibitory effect of cerivastatin is related to RhoA inactivation. This mechanism was confirmed by RhoA delocalization from cell membrane to cytoplasm and actin fiber depolymerization, which are also prevented by GGPP. It was also shown that RhoA-dependent inhibition of cell proliferation is mediated by the inhibition of focal adhesion kinase and Akt activations. Moreover, cerivastatin inhibits in vivo angiogenesis in matrigel and chick chorioallantoic membrane models. These results demonstrate the antiangiogenic activity of statins and suggest that it may contribute to their therapeutic benefits in the progression and acute manifestations of atherosclerosis. Topics: Arteriosclerosis; Cell Division; Cyclin-Dependent Kinase Inhibitor p21; Cyclins; Endothelium, Vascular; G1 Phase; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Microcirculation; Neovascularization, Pathologic; Polyisoprenyl Phosphates; Pyridines; rhoA GTP-Binding Protein; Sesquiterpenes; Signal Transduction	2002
Cracking down on caveolin: role of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors in modulating edothelial cell nitric oxide production. Circulation, 2001, Jan-02, Volume: 103, Issue:1 Topics: Arteriosclerosis; Caveolin 1; Caveolins; Cell Division; Cholesterol; Cysteine Proteinase Inhibitors; Endothelium, Vascular; GTP-Binding Proteins; Humans; Hydroxymethylglutaryl CoA Reductases; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Muscle, Smooth, Vascular; Nitric Oxide; Nitric Oxide Synthase; Nitric Oxide Synthase Type III; Polyisoprenyl Phosphates; Sesquiterpenes; Signal Transduction; Superoxides	2001

Article

Year

Cerivastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme a reductase, inhibits endothelial cell proliferation induced by angiogenic factors in vitro and angiogenesis in in vivo models.

Arteriosclerosis, thrombosis, and vascular biology, 2002, Apr-01, Volume: 22, Issue:4

Cerivastatin is an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase. It inhibits the biosynthesis of cholesterol and its precursors: farnesyl pyrophosphate and geranylgeranyl pyrophosphate (GGPP), which are involved in Ras and RhoA cell signaling, respectively. Statins induce greater protection against vascular risk than that expected by cholesterol reduction. Therefore, cerivastatin could protect plaque against rupture, an important cause of ischemic events. In this study, the effect of cerivastatin was tested on angiogenesis because it participates in plaque progression and plaque destabilization. Cerivastatin inhibits in vitro the microvascular endothelial cell proliferation induced by growth factors, whereas it has no effect on unstimulated cells. This growth arrest occurs at the G(1)/S phase and is related to the increase of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1). These effects are reversed by GGPP, suggesting that the inhibitory effect of cerivastatin is related to RhoA inactivation. This mechanism was confirmed by RhoA delocalization from cell membrane to cytoplasm and actin fiber depolymerization, which are also prevented by GGPP. It was also shown that RhoA-dependent inhibition of cell proliferation is mediated by the inhibition of focal adhesion kinase and Akt activations. Moreover, cerivastatin inhibits in vivo angiogenesis in matrigel and chick chorioallantoic membrane models. These results demonstrate the antiangiogenic activity of statins and suggest that it may contribute to their therapeutic benefits in the progression and acute manifestations of atherosclerosis.

Topics: Arteriosclerosis; Cell Division; Cyclin-Dependent Kinase Inhibitor p21; Cyclins; Endothelium, Vascular; G1 Phase; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Microcirculation; Neovascularization, Pathologic; Polyisoprenyl Phosphates; Pyridines; rhoA GTP-Binding Protein; Sesquiterpenes; Signal Transduction

2002

Cracking down on caveolin: role of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors in modulating edothelial cell nitric oxide production.

Circulation, 2001, Jan-02, Volume: 103, Issue:1

Topics: Arteriosclerosis; Caveolin 1; Caveolins; Cell Division; Cholesterol; Cysteine Proteinase Inhibitors; Endothelium, Vascular; GTP-Binding Proteins; Humans; Hydroxymethylglutaryl CoA Reductases; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Muscle, Smooth, Vascular; Nitric Oxide; Nitric Oxide Synthase; Nitric Oxide Synthase Type III; Polyisoprenyl Phosphates; Sesquiterpenes; Signal Transduction; Superoxides

2001