Comparative effects of different dihydropyridines on the expression of adhesion molecules induced by TNF-α on endothelial cells

Cominacini, Luciano; Pasini, Anna Fratta; Pastorino, Antonio M.; Garbin, Ulisse; Davoli, A.; Rigoni, Annamaria; Campagnola, M.; Tosetti, Maria; Rossato, Paolo; Gaviraghi, G.

doi:10.1097/00004872-199917121-00009

Cited by 40 publications

(36 citation statements)

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“…In the same report, it was shown that only benidipine (1 -10 μ M) inhibited TNF-induced ICAM-1 expression. It was also reported that lacidipine, lercanidipine, and amlodipine, but not nimodipine or nifedipine inhibited TNF-induced VCAM-1, ICAM-1, and e-selectin expression in HUVECs (24). In the present study, we confirmed that CV-159 (10 μ M) significantly inhibited TNF-induced expression of e-selectin but not VCAM-1 or ICAM-1 expression in HUVECs.…”

Section: Discussionsupporting

confidence: 87%

CV-159, a Unique Dihydropyridine Derivative, Prevents TNF-Induced Inflammatory Responses in Human Umbilical Vein Endothelial Cells

et al. 2010

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Abstract. CV-159, a 1,4-dihydropyridine derivative, has Ca 2+ antagonistic and anti-calmodulin actions. An early feature of atherosclerosis is vascular endothelial inflammatory change. We examined whether CV-159 has protective effects against endothelial inflammatory responses. After pretreatment of human umbilical vein endothelial cells (ECs) with CV-159 (10 μ M, 30 min), TNF-α (10 ng/ml) was applied for 20 min or 24 h. Expressions of inflammatory markers and activation of inflammatory signal molecules were examined by Western blotting. Reactive oxygen species (ROS) generation was examined by using 2′,7′-dichlorodihydrofluorescein diacetate. CV-159 inhibited TNF (24 h)-induced expression of e-selectin but not vascular cell adhesion molecule-1 and intercellular adhesion molecule-1. CV-159 inhibited TNF (20 min)-induced phosphorylation of JNK, p38, and NF-κ B p65 (Ser536). A JNK inhibitor, SP600125, and a p38 inhibitor, SB203580, inhibited TNF-induced e-selectin expression. An antioxidant drug, N -acetyl-L -cysteine (NAC), inhibited TNF-induced e-selectin expression. NAC inhibited TNF-induced phosphorylation of JNK and p38 but not NF-κ B. CV-159 inhibited TNF-induced ROS generation. Our results indicate that in ECs CV-159 specifically inhibits TNF-induced e-selectin expression through inhibition of JNK, p38, and NF-κ B phosphorylation. It is suggested that CV-159 prevents activation of JNK and p38 through inhibition of ROS, while it prevents activation of NF-κ B via a ROS-independent manner.

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Section: Discussionsupporting

confidence: 87%

CV-159, a Unique Dihydropyridine Derivative, Prevents TNF-Induced Inflammatory Responses in Human Umbilical Vein Endothelial Cells

et al. 2010

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“…Although the direct effect of gp120 on TNF-␣ expression in endothelial cells has not been determined, our data imply that TNF-␣ may not be involved in gp120-mediated endothelial ICAM-1 expression because the expression of VCAM-1 and E-selectin are not affected by gp120 treatment. Unlike HIV-1 gp120, TNF-␣ is a potent inducer for expression of all ICAM-1, VCAM-1, and E-selectin in endothelial cells (Cominacini et al, 1999;Kalogeris et al, 1999). In glial cells, inclusion of a neutralizing antibody against TNF-␣ does not block gp120-induced ICAM-1 expression, suggesting a direct effect of gp120 on ICAM-1 gene expression (Shrikant et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

HIV-1 Envelope Glycoprotein 120 Increases Intercellular Adhesion Molecule-1 Expression by Human Endothelial Cells

Ren

Yao

Chen

2002

Laboratory Investigation

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SUMMARY:Human immunodeficiency virus type 1 (HIV-1) infection is often associated with central nervous system damage and vascular complications. However, the mechanisms of this association are largely unknown. We examined the effect of HIV-1 envelope glycoprotein 120 (gp120) on cell adhesion molecule expression by endothelial cells. We found, for the first time, that both soluble and membrane-bound gp120 could significantly increase the expression of human endothelial intercellular adhesion molecule-1 (ICAM-1) at both mRNA and protein levels, but not vascular cell adhesion molecule-1 and E-selectin. The specificity of gp120-mediated response was demonstrated by blocking experiments using a specific monoclonal antibody against gp120, which successfully abolished the gp120-mediated increase of ICAM-1 expression. Furthermore, there was a significant increase of human monocytic cell line THP-1 adherence onto the gp120-treated endothelial monolayers. This increased cell adhesion was effectively blocked by either anti-gp120 or anti-ICAM antibodies. These findings suggest that HIV-1 gp120-mediated endothelial ICAM-1 expression could be one of the important mechanisms of HIV-1 pathogenesis. (Lab Invest 2002, 82:245-255). B oth human immunodeficiency virus (HIV)-positiveand acquired immune deficiency syndrome (AIDS) patients often have significantly increased levels of circulating cell adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) (Greenwood et al, 1998; Seigneur et al, 1997). Serum ICAM-1 levels correlate well with AIDS progression in HIV type 1 (HIV-1)-infected patients (Galea et al, 1997). Endothelial cells and leukocytes from these patients exhibit a significant increase of such adhesion molecules (Pillet et al, 1999;Zietz et al, 1996). HIV-1 particles also incorporate many cell adhesion molecules (Guo and Hildreth, 1995). HIV-associated ICAM-1 is biologically active and can enhance virus infectivity (Fortin et al, 1997) and virus-induced syncytium formation (Gruber et al, 1991). ICAM-1-bearing viruses are less susceptible to neutralization by anti-envelope glycoprotein 120 (gp120) monoclonal antibodies than the same virus produced in cells expressing no ICAM-1 (Sawyer et al, 1994). HIV-1 replication in monocytes/macrophages is significantly enhanced by interaction with endothelial cells through cell adhesion molecules (Gilles et al, 1995). In addition, alterations in expression of cell adhesion molecules by leukocytes and endothelial cells can increase leukocyte migration into the tissues, which may result in certain organ damage. Indeed, HIV-1-infected leukocytes can transmigrate into the central nervous system and cause encephalopathy (Nottet, 1999). Endothelial cell dysfunction and leukocyte infiltration may also be attributable to the increased frequency of vascular complications such as atherosclerosis in HIV-1-infected patients (Constans et al, 1995;Tabib et al, 2000).Several factors may contribute to the increased levels of cell adhesion mole...

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“…The calcium channel blockade amlodipine has been shown to limit the progression of arteriosclerosis and atherosclerosis in animals and humans (37,38). Although the mechanisms underlying the direct protective effects of calcium channel blockades on endothelial cell injury are not fully understood, such vasoprotective effects as the amelioration of endothelial dysfunction (39,40) and decreases in the proliferation of vascular smooth muscle cells (41), oxidative stress (37,42), and inflammation (43), are at least in part independent of the blood pressure-lowering effects of these agents. The calcium channel blockade has been shown to ameliorate hypertension and improve NO production in the vasculature and kidneys.…”

Section: Introductionmentioning

confidence: 99%

Calcium Channel Blockades Exhibit Anti-Inflammatory and Antioxidative Effects by Augmentation of Endothelial Nitric Oxide Synthase and the Inhibition of Angiotensin Converting Enzyme in the NG-Nitro-L-Arginine Methyl Ester-Induced Hypertensive Rat Aorta: Vasoprotective Effects beyond the Blood Pressure-Lowering Effects of Amlodipine and Manidipine

et al. 2005

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Comparative effects of different dihydropyridines on the expression of adhesion molecules induced by TNF-α on endothelial cells

Abstract: It is concluded that the effect of the DHPs used in this study on adhesion molecule expression is determined first by their lipophilicity and then by their intrinsic antioxidant activity.

Cited by 40 publications

References 36 publications

CV-159, a Unique Dihydropyridine Derivative, Prevents TNF-Induced Inflammatory Responses in Human Umbilical Vein Endothelial Cells

CV-159, a Unique Dihydropyridine Derivative, Prevents TNF-Induced Inflammatory Responses in Human Umbilical Vein Endothelial Cells

HIV-1 Envelope Glycoprotein 120 Increases Intercellular Adhesion Molecule-1 Expression by Human Endothelial Cells

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