Acute-phase response to benzo[a]pyrene and induction of rat ALDH3A1

Pappas, Periklis; Sotiropoulou, Marianthi; Karamanakos, Petros N; Kostoula, Angeliki; Levidiotou, Stamatia; Marselos, Marios

doi:10.1016/s0009-2797(02)00172-2

Cited by 12 publications

(5 citation statements)

References 13 publications

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“…ALDH1A3 is also a xenobiotic response gene but classically is induced by phenobarbital-like P450 inducers, while a related enzyme, ALDH3A1, not seen in this study, is associated with AhR-mediated responses (52). In addition to being an AhRresponsive gene, PTGS2 is strongly induced in endothelium by IL-1␤ (20).…”

Section: Discussionmentioning

confidence: 78%

Comparative gene responses to collected ambient particles in vitro: endothelial responses

Aung

Lamé²,

Gohil³

et al. 2011

Physiological Genomics

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Epidemiologic studies associate exposure to ambient particulate matter (APM) with increased cardiovascular mortality. Since both pulmonary inflammation and systemic circulation of ultrafine particles are hypothesized as initiating cardiovascular effects, we examined responses of potential target cells in vitro. Human aortic endothelial cells (HAEC) were exposed to 10 μg/ml fine and ultrafine APM collected in an urban setting in summer 2006 or winter 2007 in the San Joaquin Valley, California. RNA isolated after 3 h was analyzed with high-density oligonucleotide arrays. Summer APM treatment affected genes involved in xenobiotic and oxidoreductase activity, transcription factors, and inflammatory responses in HAEC, while winter APM had a robust xenobiotic but lesser inflammatory response. Real-time polymerase chain reaction analysis confirmed that particulate matter (PM)-treated HAEC increased mRNA levels of xenobiotic response enzymes CYP1A1, ALDH1A3, and TIPARP and cellular stress response transcription factor ATF3. Inflammatory response genes included E-selectin, PTGS2, CXCL-2 (MIP-2α), and CCL-2 (MCP-1). Multiplex protein assays showed secretion of IL-6 and MCP-1 by HAEC. Since induction of CYP1A1 is mediated through the ligand-activated aryl hydrocarbon receptor (AhR), we demonstrated APM induced AhR nuclear translocation by immunofluorescence and Western blotting and activation of the AhR response element using a luciferase reporter construct. Inhibitor studies suggest differential influences of polycyclic aromatic hydrocarbon signaling, ROS-mediated responses and endotoxin alter stress and proinflammatory endothelial cell responses. Our findings demonstrate gene responses correlated with current concepts that systemic inflammation drives cardiovascular effects of particulate air pollution. We also demonstrate a unique pattern of gene responses related to xenobiotic metabolism in PM-exposed HAEC.

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Section: Discussionmentioning

confidence: 78%

Comparative gene responses to collected ambient particles in vitro: endothelial responses

Aung

Lamé²,

Gohil³

et al. 2011

Physiological Genomics

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“…Elevation of [Ca 2ϩ ] i in response to AhR agonists has been reported in various cellular models, including lymphocytes (Burchiel et al, 1991;Pallardy et al, 1992;Archuleta et al, 1993), macrophages (NЈDiaye et al, 2006;Pappas et al, 2003), intestinal (Le Ferrec et al, 2002), and mammary cells (Tannheimer et al, 1997) and can therefore be considered a hallmark of AhR agonist exposure. It is noteworthy that this change of [Ca 2ϩ ] i has been recently demonstrated to be required for regulation of the AhR target genes CYP1A1 and CCL1, in human Caco-2 intestinal cells (Le Ferrec et al, 2002) and human macrophages (NЈDiaye et al, 2006), respectively.…”

Section: Discussionmentioning

confidence: 99%

Dioxin-Mediated Up-Regulation of Aryl Hydrocarbon Receptor Target Genes Is Dependent on the Calcium/Calmodulin/CaMKIα Pathway

Monteiro

Gilot²,

Ferrec

et al. 2007

Mol Pharmacol

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“…It has been reported that the levels of proinflammatory cytokines, such as interleukin 1 (IL-1) and C-reactive protein, circulating markers of inflammation, correlated well with βG activity in the serum of patients with inflammatory disorders (20). Published data (22) add in vivo human evidence to previous animal data ( [23][24][25][26][27] that βG is a potential biomarker useful for monitoring pulmonary inflammation caused by human exposure to coal dust, asbestos fibers, crystalline silica dust, diesel engine exhaust, and tobacco smoke. In a murine model, concomitant with the morphologic changes noted with the increasing duration of tobacco smoke exposure, the alveolar and pulmonary macrophage population size increased approximately 8-fold compared to the control values.…”

Section: Dietary D-glucarate Effects On the Biomarkers Of Inflammatiomentioning

confidence: 91%

Dietary D-glucarate effects on the biomarkers of inflammation during early post-initiation stages of benzo[a]pyrene-induced lung tumorigenesis in A/J mice

Zoltaszek

Kowalczyk

et al. 2010

Oncol Lett

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Abstract. Previous studies showed that dietary calcium D-glucarate (CG) inhibited benzo[a]pyrene (B[a]P)-inducedA/J mouse lung tumorigenesis, suppressing cell proliferation and chronic inflammation and inducing apoptosis during late post-initiation stages. The present study aimed to investigate changes in the homeostasis of cytokines in blood serum, as well as alterations in biomarkers of inflammation and apoptosis in lung tissue caused by dietary CG during early post-initiation stages of B[a]P-induced lung tumorigenesis. Two doses of 3 mg of B[a]P were given intragastrically to A/J mice 2 weeks apart. CG administration in the AIN-93G diet (2 and 4%, w/w) commenced at 2 weeks following the second dose of B[a]P. The levels of interleukin (IL)-6, IL-10 and tumor necrosis factor α (TNFα) in blood serum were investigated by FCAP array analysis. Two weeks after the second dose of B[a]P, approximately 8-and 28-fold increases of TNFα and IL-6, respectively, occurred in the blood serum and an approximately 16% decrease of IL-10 levels compared to the untreated control group was noted. At 4 weeks after the second dose of B[a]P and after 2 weeks of CG administration in the diet, the 2 and 4% CG diets significantly reduced the levels of IL-6 and TNFα (by 70 and 33%, respectively). In a dose-related manner, the diets also increased the level of antiinflammatory cytokine IL-10 compared to the B[a]P group. At 6 weeks after the second dose of B[a]P, the cytokine levels in the serum continued to show a decrease in the CG-treated groups. These events are accompanied by an increased level of cleaved caspase-9 product with a molecular weight of 37 kDa. In conclusion, dietary D-glucarate decreases the level of proinflammatory cytokines, increases the level of the anti-inflammatory cytokine IL-10 during early post-initiation stages of B[a]P-induced lung tumorigenesis in A/J mice and affects apoptotic induction.

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Acute-phase response to benzo[a]pyrene and induction of rat ALDH3A1

Cited by 12 publications

References 13 publications

Comparative gene responses to collected ambient particles in vitro: endothelial responses

Comparative gene responses to collected ambient particles in vitro: endothelial responses

Dioxin-Mediated Up-Regulation of Aryl Hydrocarbon Receptor Target Genes Is Dependent on the Calcium/Calmodulin/CaMKIα Pathway

Dietary D-glucarate effects on the biomarkers of inflammation during early post-initiation stages of benzo[a]pyrene-induced lung tumorigenesis in A/J mice

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