Heavy-metal modulation of the human intercellular adhesion molecule (ICAM-1) gene expression

Martinotti, Stefano; Toniato, E; Colagrande, Antonella; Alesse, Edoardo; Alleva, Claudia; Screpanti, Isabella; Morrone, Stefania; Scarpa, Susanna; Frati, Luigi; Hayday, Adrian; Piovella, Franco; Gulino, Alberto

doi:10.1016/0167-4781(94)00237-w

Cited by 26 publications

(13 citation statements)

References 36 publications

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“…It has been reported that ICAM-1 gene expression is associated with Cd-induced injury in various tissues (Martinotti et al, 1995;Jiang et al, 2002;Mousa, 2004). Thus, our findings imply the possible role of COX-2 expression on brain endothelial cells in Cdinduced CNS injury, though additional in vitro and in vivo studies are needed to confirm functional significance of results from this study.…”

Section: Discussionsupporting

confidence: 62%

“…Cd induces COX-2 expression and enhances lipid peroxidation and PGE 2 synthesis in several experimental models (Romare and Lundholm, 1999;Ramirez and Gimenez, 2003). Cd-induced proinflammatory changes also include upregulation of intercellular adhesion molecule-1(ICAM-1) which has been implicated in inflammatory tissue injury (Martinotti et al, 1995;Jiang et al, 2002;Mousa, 2004). Very recently, we have shown that Cd stimulates the expression of ICAM-1 via NF-B activation in cerebrovascular endothelial cells (Jeong et al, 2004).…”

Section: Introductionmentioning

confidence: 98%

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COX-2 is associated with cadmium-induced ICAM-1 expression in cerebrovascular endothelial cells

et al. 2006

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Section: Discussionsupporting

confidence: 62%

Section: Introductionmentioning

confidence: 98%

COX-2 is associated with cadmium-induced ICAM-1 expression in cerebrovascular endothelial cells

et al. 2006

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“…Zinc deficiency in mast cell prevented activation of PKC and nuclear factor B, resulting in reduction of cytokine production (Kabu et al, 2006). Previous studies reported that zinc treatment induces intercellular adhesion molecule-1 expression in endothelial cells (Martinotti et al, 1995) and leukocyte adhesion (Klein et al, 1994;Chavakis et al, 1999). Furthermore, a potential role of zinc in inflammatory signaling is proposed in monocytes (Haase and Rink, 2007).…”

Section: Downloaded Frommentioning

confidence: 94%

Angiotensin-Converting Enzyme Inhibitor Attenuates Monocyte Adhesion to Vascular Endothelium through Modulation of Intracellular Zinc

Kojima¹,

Kawakami²,

Takei³

et al. 2007

J Pharmacol Exp Ther

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To elucidate an anti-inflammatory role of angiotensin-converting enzyme inhibitors (ACEIs) in cardiovascular disease, we studied the effect of ACEIs in monocyte adhesion to endothelial cells and underlying molecular mechanisms. Treatment of human monocytic THP-1 cells with monocyte chemoattractant protein-1 (MCP-1; 100 ng/ml; 10 min) significantly increased their adhesion to human umbilical vein endothelial cells (HUVECs) under flow condition (P Ͻ 0.001). Preincubation of THP-1 cells with imidaprilat (50 nM; 4 h), an active metabolite of imidapril, reduced MCP-1-triggered THP-1 cell adhesion (P Ͻ 0.01). Similar effects were obtained with experiments using human peripheral monocytes (P Ͻ 0.05). MCP-1 activated protein kinase C (PKC)␣ in THP-1 cells, resulting in the up-regulation of ␣4 and ␤2 integrin. Imidaprilat attenuated MCP-1-induced PKC activation and integrin up-regulation in THP-1 cells.Imidaprilat also inhibited THP-1 cell adhesion induced by phorbol 12-myristate 13-acetate (PMA), a potent PKC activator. In attempt to elucidate the mechanisms for the modulation of PKC activity by imidaprilat, we found that MCP-1 or PMA increased labile zinc in THP-1 cells, which was canceled by imidaprilat. Indeed, zinc/pyrithione activated PKC and increased THP-1 cell adhesion. Zinc chelator as well as PKC inhibitor inhibited these processes, suggesting the role for labile zinc in PKC activation and THP-1 cell adhesion. Imidaprilat attenuated zinc/pyrithione-induced PKC activation and THP-1 cell adhesion. These data suggest that ACEI reduces MCP-1 or PMA-triggered monocyte adhesion to activated HUVECs by modulating labile zinc in monocytes. Our findings may point out a novel antiinflammatory mechanism of ACEIs in atherogenesis.

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“…This finding has been previously reported in different nephropathies (Daniel et al, 2001;Fernandez et al, 2003), suggesting that tubular ICAM-1 expression may represent a common event during renal injury. Interestingly, cadmium and mercury induce endothelial ICAM-1 gene expression in humans and ICAM-1 expression on immortalized proximal tubule cells (Martinotti et al, 1995;Pritchard et al, 2000;Jiang et al, 2002). The over-expression of ICAM-1 in proximal tubules could be a deleterious factor, since it has been associated to apoptosis and proliferation during experimental nephropathy (Shappell et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Pro-inflammatory role of angiotensin II in mercuric chloride-induced nephropathy in rats

Peña

Hernández-Fonseca

Rincón

et al. 2012

Journal of Immunotoxicology

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Heavy-metal modulation of the human intercellular adhesion molecule (ICAM-1) gene expression

Cited by 26 publications

References 36 publications

COX-2 is associated with cadmium-induced ICAM-1 expression in cerebrovascular endothelial cells

COX-2 is associated with cadmium-induced ICAM-1 expression in cerebrovascular endothelial cells

Angiotensin-Converting Enzyme Inhibitor Attenuates Monocyte Adhesion to Vascular Endothelium through Modulation of Intracellular Zinc

Pro-inflammatory role of angiotensin II in mercuric chloride-induced nephropathy in rats

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