Lovastatin-stimulated superinduction of E-selectin, ICAM-1 and VCAM-1 in TNF-α activated human vascular endothelial cells

Schmidt, Annette; Goepfert, Christian; Feitsma, Kirsten; Buddecke, Eckhart

doi:10.1016/s0021-9150(02)00053-9

Cited by 55 publications

(41 citation statements)

References 25 publications

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“…This difference is considered to be due to differences in the permeability of the cell membrane based on the lipid solubility of simvastatin and water solubility of pravastatin. Other effects for HMG-CoA RIs were also reported, including suppression of the oxidation of LDL (15), suppression of the super induction of chemotaxic factors (16) and adhesion factors (17)(18)(19), and a reduction in the accumulation of oxidized LDL in macrophages (20). We believe that these modes of actions of HMG-CoA RIs interacted in a complex manner to reduce IMT of the carotid artery in our patients treated with simvastatin or pravastatin.…”

Section: Discussionsupporting

confidence: 59%

HMG-CoA Reductase Inhibitors Suppress the Development and Progression of Carotid Artery Intimal-medial Thickening in Hypercholesterolemic Type 2 Diabetic Patients

Takahashi

Ishii

Itai

et al. 2005

JAT

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We reported previously that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (RIs) suppressed in vitro oxidized-low density lipoprotein-induced macrophage growth. To elucidate whether HMG-CoA RIs have anti-atherogenic effects separate from their cholesterol-lowering effect, total plasma levels of cholesterol in patients with type 2 diabetes mellitus (type 2 DM) and hypercholesterolemia were reduced to normal by one-year treatment with HMG-CoA RIs and intimal-medial thickness (IMT) of the common carotid arteries (CCA) was measured. Patients with type 2 DM and hypercholesterolemia received either pravastatin (n = 15) or simvastatin (n = 15), while another group of type 2 DM patients with normocholesterolemia did not receive these agents. IMT of the CCA was measured using Powervision SSA-370A, probe 7.5 Mhz. The mean IMT and the rate of increase of IMT were relatively elevated in the order of the simvastatin-treatment group, pravastatin-treatment group, and control group. Our results suggested that HMG-CoA RIs might have anti-atherogenic effects in addition to their cholesterol-lowering effect. J Atheroscler Thromb, 2005; 12: 149-153.

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Section: Discussionsupporting

confidence: 59%

HMG-CoA Reductase Inhibitors Suppress the Development and Progression of Carotid Artery Intimal-medial Thickening in Hypercholesterolemic Type 2 Diabetic Patients

Takahashi

Ishii

Itai

et al. 2005

JAT

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“…Statins are known to attenuate the recruitment of circulating leukocytes to endothelium including leukocytes rolling, adhesion, and transmigration [2,4,5,15,27], which represents a hallmark of vascular inflammation. Previous studies are limited to the impact of statins on ICAM-1, VCAM-1, E-selectin and P-selectin [2,16,17,27,28] which are inducible endothelial CAMs with functional relevance confined to leukocyte tethering and adhesion [29].…”

Section: Discussionmentioning

confidence: 99%

“…[16,17], which are involved in leukocytes tethering and adhesion to endothelium, the mechanism of statinsÕ inhibitory effect on TEM at the molecular level, however, has yet to be explored.…”

Section: Introductionmentioning

confidence: 99%

Statin‐inhibited endothelial permeability could be associated with its effect on PECAM‐1 in endothelial cells

Wei¹,

Lü²,

Song³

et al. 2005

FEBS Letters

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The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) are known to inhibit leukocyte recruitment to endothelium but the mechanism is less understood. Platelet endothelial cell adhesion molecule-1 (PECAM-1) is an endothelial junction protein involved in leukocyte diapedesis. We hypothesize that in endothelial cells, statins may well recruit PECAM-1 to exert their inhibitory effect on leukocyte transendothelial migration (TEM). In lovastatin-treated resting human umbilical vein endothelial cells (HUVECs), increased levels of mRNA and protein of PECAM-1 as well as its bio-synthesis (all 2-fold) were observed by real-time PCR, Western blotting and 35 S-labeled methionine incorporation assay, respectively. Moreover, in lovastatin treated resting cells as well as TNF-a activated endothelial cells, unanimously decreased Triton X-100 insoluble and soluble PECAM-1 ratio was observed. Such changes were accompanied by decreased TEM of U-937 cells (a promonocyte cell line). All lovastatinÕs effects were abrogated by mevalonic acid. In resting HUVECs, geranylgeranyl pyrophosphate (GGPP), but not farnesyl pyrophosphate (FPP) (both are isoprenoid intermediates in the cholesterol biosynthesis pathway) compromised the effect of lovastatin on PECAM-1 expression, whereas C3 toxin, an inhibitor of small G proteins, exerted statin-like effect.Conclusion: Statin-reduced endothelial permeability could be attributed to altered intracellular distribution of PECAM-1 in endothelial cells. We speculate that lovastatin regulates PE-CAM-1 expression in HUVECs through the mevalonate-GGPP pathway by inhibiting of Rho small GTPase.

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“…Incubation of HUVECs with IL-1␤ and TNF-␣ induced upregulation of E-selectin and ICAM-1 after 4 -6 h (Figs. 2 and 3), a time at which these molecules are usually upregulated by these proinflammatory cytokines (8,76). Cytokine-mediated upregulation of adhesion molecules has been well characterized in HUVECs (44,61,77).…”

Section: Hsg Cells Express Lxamentioning

confidence: 99%

Lipoxin A₄ inhibits immune cell binding to salivary epithelium and vascular endothelium

Chinthamani

Odusanwo

Mondal

et al. 2012

American Journal of Physiology-Cell Physiology

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Lovastatin-stimulated superinduction of E-selectin, ICAM-1 and VCAM-1 in TNF-α activated human vascular endothelial cells

Cited by 55 publications

References 25 publications

HMG-CoA Reductase Inhibitors Suppress the Development and Progression of Carotid Artery Intimal-medial Thickening in Hypercholesterolemic Type 2 Diabetic Patients

HMG-CoA Reductase Inhibitors Suppress the Development and Progression of Carotid Artery Intimal-medial Thickening in Hypercholesterolemic Type 2 Diabetic Patients

Statin‐inhibited endothelial permeability could be associated with its effect on PECAM‐1 in endothelial cells

Lipoxin A₄ inhibits immune cell binding to salivary epithelium and vascular endothelium

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Lovastatin-stimulated superinduction of E-selectin, ICAM-1 and VCAM-1 in TNF-α activated human vascular endothelial cells

Cited by 55 publications

References 25 publications

HMG-CoA Reductase Inhibitors Suppress the Development and Progression of Carotid Artery Intimal-medial Thickening in Hypercholesterolemic Type 2 Diabetic Patients

HMG-CoA Reductase Inhibitors Suppress the Development and Progression of Carotid Artery Intimal-medial Thickening in Hypercholesterolemic Type 2 Diabetic Patients

Statin‐inhibited endothelial permeability could be associated with its effect on PECAM‐1 in endothelial cells

Lipoxin A4 inhibits immune cell binding to salivary epithelium and vascular endothelium

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Lipoxin A₄ inhibits immune cell binding to salivary epithelium and vascular endothelium