The environmental carcinogen benzo[a]pyrene induces expression of monocyte-chemoattractant protein-1 in vascular tissue: a possible role in atherogenesis

Knaapen, Ad M.; Curfs, Daniëlle M. J.; Pachen, D. M. F. A.; Gottschalk, Ralph W.H.; Winther, Menno P.J. de; Daemen, Mat J.A.P.; Schooten, Frederik J. van

doi:10.1016/j.mrfmmm.2006.12.010

Cited by 60 publications

(38 citation statements)

References 45 publications

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“…24 Benzo (a) pyrene also upregulates atherosclerotic plaque formation in the ApoE knock out mouse and induces MCP-1 expression in HUVECs through AhR activation. 31 Additionally, CYP1A1, which is induced by TCDD, promotes ROS generation in human aortic endothelial cells and decreases nitric oxide (NO) production, indicating that AhR activation induces endothelial dysfunction. 32 These studies suggest that ligand-activated AhR induces a response in cardiovascular cells, although there are other potential ago- 9 However, in our experimental setting, probenecid failed to prevent MCP-1 and Nox4 expressions in HUVECs with IS treatment.…”

Section: Discussionmentioning

confidence: 99%

Activation of Aryl Hydrocarbon Receptor Mediates Indoxyl Sulfate-Induced Monocyte Chemoattractant Protein-1 Expression in Human Umbilical Vein Endothelial Cells

Watanabe

Tatebe

Namba

et al. 2013

Circ J

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp positive correlation between chronic kidney disease (CKD) and cardiovascular disease (CVD) has been demonstrated, but the causative role of uremic toxin remains unclear. 1-3 A number of retention compounds act as uremic toxins, accumulating in the blood of CKD patient, and elevated circulating uremic toxins negatively affect biological function through induction of oxidative stress. The removal of uremic solutes, therefore, has the potential to prevent CVD. However, protein-bound retention solutes are insufficiently eliminated even by hemodialysis. 4-6 Indoxyl sulfate (IS) is a protein-bound uremic toxin metabolized in the liver from indole, a tryptophan metabolite that is formed by intestinal bacteria. Together with CKD progression, IS accumulates in the blood, which leads to cellular toxicity by inducing oxidative stress. 7In particular, recent studies have suggested that IS is associated with vascular damage by inducing vasoactive substances related to atherogenesis such as chemokines, cytokines or cell adhesion molecules. 8,9 As a possible mechanism of the process, we previously demonstrated that IS mediates monocyte chemoattractant protein-1 (MCP-1) expression in human umbilical vein endothelial cells (HUVECs) by producing reactive oxygen species (ROS) through NADPH oxidase activation. 10 MCP-1 is a chemokine that is involved in early stage of atherosclerosis through the recruitment of monocytes from the blood stream to the subendothelial space. 11-13 Moreover, others have shown that IS-induced vascular damage exhibits inflammatory effects in monocytes, vascular smooth muscle cells or cardiac myocytes.

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Section: Discussionmentioning

confidence: 99%

Activation of Aryl Hydrocarbon Receptor Mediates Indoxyl Sulfate-Induced Monocyte Chemoattractant Protein-1 Expression in Human Umbilical Vein Endothelial Cells

Watanabe

Tatebe

Namba

et al. 2013

Circ J

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“…In vitro studies with human endothelial cells (RF24 cell line and primary HUVEC), indicated that acute exposure to B(a)P causes a doseand time-dependent cell toxicity (Knaapen AM, 2007). Furthermore, Chaudhary et al, recently reported production of reactive oxygen species in both 22Rv1 and PrEC cells upon exposure to acute B(a)P leading to cell toxicity (Chaudhary et al, 2007).…”

Section: B(a)p-induced Suppression Of Temporal Developmental Expressimentioning

confidence: 99%

Down-regulation of early ionotrophic glutamate receptor subunit developmental expression as a mechanism for observed plasticity deficits following gestational exposure to benzo(a)pyrene

et al. 2007

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The focus of this study was to characterize the impact of gestational exposure to benzo(a)pyrene, [B (a)P] on modulation of glutamate receptor subunit expression that is critical for the maintenance of synaptic plasticity mechanisms during hippocampal or cortical development in offspring. Previous studies have demonstrated that hippocampal and/or cortical synaptic plasticity (as measured by longterm potentiation and S1-cortex spontaneous/evoked neuronal activity) and learning behavior (as measured by fixed-ratio performance operant testing) is significantly impaired in polycyclic aromatic or halogenated aromatic hydrocarbon-exposed offspring as compared to controls. These previous studies have also revealed that brain to body weight ratios are greater in exposed offspring relative to controls indicative of intrauterine growth retardation which has been shown to manifest as low birth weight in offspring. Recent epidemiological studies have identified an effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the first 3 Years of life among inner-city children (Perera et al., 2006). The present study utilizes a well-characterized animal model to test the hypothesis that gestational exposure to B(a)P causes dysregulation of developmental ionotropic glutamate receptor subunit expression, namely the N-methyl-D-aspartate receptor (NMDAR) and α-amino-3-hydroxy-5-methyl-4-isoxazole-propionate receptor (AMPAR) both critical to the expression of synaptic plasticity mechanisms. To mechanistically ascertain the basis of B(a)P-induced plasticity perturbations, timed pregnant Long-Evans rats were exposed in an oral subacute exposure regimen to 0, 25 and 150µg/kg BW B(a)P on gestation days 14-17. The first sub-hypothesis tested whether gestational exposure to B(a)P would result in significant disposition in offspring. The second sub-hypothesis tested whether gestational exposure to B(a)P would result in downregulation of early developmental expression of NMDA and AMPA receptor subunits in the *Corresponding author: Darryl B. Hood, Ph.D., Department of Neurobiology and Neurotoxicology, Center for Molecular and Behavioral Neuroscience, Meharry Medical College, Nashville, TN 37208, USA. Phone (615) 327-6358, FAX: (615) 327-6632. email: dhood@mmc.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. hippocampus of offspring as well as in primary neuronal cultures. The results of these studies revealed significant: 1) disposition to the hippocampus and cortex, 2) down-regulation of developmental glutamate receptor mRNA and protein subunit expres...

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“…Although well-known lifestyle factors such as diet, smoking, and lack of exercise are viewed as the major influences, accumulating evidence suggests that exposure to environmental pollutants and chemicals has an association with atherogenesis (Pope III et al 2004;Brook et al 2004;Knaapen et al 2007). The American Heart Association (AHA) published an AHA scientific statement in ''Circulation' ' (2004) declaring that air pollution is a ''serious public health problem'' for CVD (Brook et al 2004).…”

Section: Introductionmentioning

confidence: 99%

Inflammatory responses induced by fluoride and arsenic at toxic concentration in rabbit aorta

Niu

Sun

et al. 2012

Arch Toxicol

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Epidemiological and experimental studies have demonstrated the atherogenic effects of environmental toxicant arsenic and fluoride. Inflammatory mechanism plays an important role in the pathogenesis of atherosclerosis. The aim of the present study is to determine the effect of chronic exposure to arsenic and fluoride alone or combined on inflammatory response in rabbit aorta. We analyzed the expression of genes involved in leukocyte adhesion [P-selectin (P-sel) and vascular cell adhesion molecule-1(VCAM-1)], recruitment and transendothelial migration of leukocyte [interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1)] and those involved in pro-inflammatory cytokines [interleukin-6 (IL-6)]. We found that fluoride and arsenic alone or combined increased the expression of VCAM-1, P-sel, MCP-1, IL-8, and IL-6 at the RNA and protein levels. The gene expressions of inflammatory-related molecules were attenuated when co-exposure to the two toxicants compared with just one of them. We also examined the lipid profile of rabbits exposed to fluoride and (or) arsenic. The results showed that fluoride slightly increased the serum lipids but arsenic decreased serum triglyceride. We showed that inflammatory responses but not lipid metabolic disorder may play a crucial role in the mechanism of the cardiovascular toxicity of arsenic and fluoride.

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The environmental carcinogen benzo[a]pyrene induces expression of monocyte-chemoattractant protein-1 in vascular tissue: a possible role in atherogenesis

Cited by 60 publications

References 45 publications

Activation of Aryl Hydrocarbon Receptor Mediates Indoxyl Sulfate-Induced Monocyte Chemoattractant Protein-1 Expression in Human Umbilical Vein Endothelial Cells

Activation of Aryl Hydrocarbon Receptor Mediates Indoxyl Sulfate-Induced Monocyte Chemoattractant Protein-1 Expression in Human Umbilical Vein Endothelial Cells

Down-regulation of early ionotrophic glutamate receptor subunit developmental expression as a mechanism for observed plasticity deficits following gestational exposure to benzo(a)pyrene

Inflammatory responses induced by fluoride and arsenic at toxic concentration in rabbit aorta

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