2001
DOI: 10.1161/hq0701.092143
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HMG-CoA Reductase Inhibitor Modulates Monocyte–Endothelial Cell Interaction Under Physiological Flow Conditions In Vitro

Abstract: Abstract-3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, or statins, have been reported to exert actions independent of their lipid-lowering effects. To critically assess the effects of statins on monocyte-endothelial cell interactions, we used an in vitro model that mimicked physiological flow conditions. Monocytic U937 cells were incubated in the presence of cerivastatin for 48 hours.

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Cited by 173 publications
(169 citation statements)
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“…This suggests that atorvastatin, via reduction of RAC1 and RHOA activity associated with a reduction in cardiac oxidative stress and increased eNOS levels, reduces inflammation in diabetic cardiomyopathy. This hypothesis is supported by the finding that: (1) monocyte adhesion to vascular endothelium is reduced via statin-mediated downregulation of integrin adhesion molecules and inhibition of actin polymerisation via RHOA inactivation [40]; (2) atorvastatin treatment inhibits glucose-mediated neutrophil-endothelial Fig. 6 Effect of atorvastatin treatment (Ator) on eNOS levels in STZdiabetic rat hearts.…”
Section: Effect Of Atorvastatin On Lipid Profilementioning
confidence: 85%
See 1 more Smart Citation
“…This suggests that atorvastatin, via reduction of RAC1 and RHOA activity associated with a reduction in cardiac oxidative stress and increased eNOS levels, reduces inflammation in diabetic cardiomyopathy. This hypothesis is supported by the finding that: (1) monocyte adhesion to vascular endothelium is reduced via statin-mediated downregulation of integrin adhesion molecules and inhibition of actin polymerisation via RHOA inactivation [40]; (2) atorvastatin treatment inhibits glucose-mediated neutrophil-endothelial Fig. 6 Effect of atorvastatin treatment (Ator) on eNOS levels in STZdiabetic rat hearts.…”
Section: Effect Of Atorvastatin On Lipid Profilementioning
confidence: 85%
“…Effect of atorvastatin on intramyocardial inflammation Many of the pleiotropic effects of statins are mediated by antagonism of isoprenoid-mediated activation of small GTP-binding proteins, including RAC1 and RHOA [11], which have previously been suggested to be mediators of inflammation [23,40]. Both RAC1 [41] and RHOA GTPase [42] are involved in the regulation of the cytoskeleton network, which includes integrin-dependent leucocyte adhesion.…”
Section: Effect Of Atorvastatin On Lipid Profilementioning
confidence: 99%
“…Statins have been reported to inhibit interactions between leukocytes and endothelial cells (ECs) that necessarily precede leukocyte egress from the vasculature (26)(27)(28). Different groups of adhesion molecules sequentially mediate leukocyte rolling, adhesion, and diapedesis, or transmigration through the vascular wall (29).…”
Section: Statins As Antiinflammatory Drugs: Effects On Cells and Tissuesmentioning
confidence: 99%
“…As the authors discussed, active inflammation induced by intermittent hypoxia may have a role in the development of left ventricular remodeling. Numerous studies, including ours, 11,12 point to an anti-inflammatory role of statins in addition to their lipid-lowering effects. Therefore, the anti-inflammatory potential of statins may be beneficial in treating left ventricular hypertrophy.…”
mentioning
confidence: 80%