Inhibition of basal and interleukin-1-induced VCAM-1 expression by phospholipid hydroperoxide glutathione peroxidase and 15-lipoxygenase in rabbit aortic smooth muscle cells

Banning, Antje; Schnurr, Kerstin; Böl, Gaby Fleur; Kupper, Dagmar; Müller-Schmehl, Katrin; Viita, Helena; Ylä‐Herttuala, Seppo; Brigelius‐Flohé, Regina

doi:10.1016/j.freeradbiomed.2003.10.027

Cited by 33 publications

(23 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Overexpression of Cu/Zn-SOD and catalase in vascular smooth muscle cells has been shown to inhibit VCAM-1 expression through inhibition of NF-κB [31]. The present study demonstrates that overexpression of Cu/Zn-SOD and catalase efficiently reduces BaP-induced ROS in MAECs.…”

Section: Discussionsupporting

confidence: 58%

See 1 more Smart Citation

Overexpression of antioxidant enzymes in ApoE-deficient mice suppresses Benzo(a)pyrene-accelerated atherosclerosis

et al. 2009

View full text Add to dashboard Cite

The carcinogenic polycylic aromatic hydrocarbon, benzo(a)pyrene (BaP), has been shown to generate reactive oxygen species (ROS) and accelerate the development of atherosclerosis. To assess the causal role of BaP-generated ROS in this process, we evaluated atherosclerotic metrics in apolipoprotein E-deficient (ApoE-/-) mice with or without overexpression of Cu/Zn-superoxide dismutase (Cu/Zn-SOD) and/or catalase. Without BaP, aortic atherosclerotic lesions were smaller in ApoE-/- mice overexpressing catalase or both Cu/Zn-SOD and catalase than in those overexpressing neither or Cu/Zn-SOD only. After treating with BaP or vehicle for 24 weeks, mean lesion sizes in the aortic tree and aortic root of ApoE-/- mice were increased by approximately 60% and 40%, respectively. BaP also increased the levels of oxidized lipids in the aortic tree of ApoE-/- mice and increased the frequency of advanced lesions. In contrast, BaP did not significantly alter lipid peroxidation levels or atherosclerotic lesions in the aortas of ApoE-/- mice overexpressing Cu/Zn-SOD and/or catalase. Overexpression of Cu/Zn-SOD and/or catalase also inhibited BaP-induced expression of cell adhesion molecules in aortas and endothelial cells, and reduced BaP-induced monocyte adhesion to endothelial cells. These observations, together with the functions of catalase and Cu/Zn-SOD to scavenge hydrogen peroxide and superoxide anions, implicate a causal role of ROS in the pathogenesis of BaP-induced atherosclerosis.

show abstract

Section: Discussionsupporting

confidence: 58%

“…It is well established that ROS induce cell adhesion molecule expression by activation of redox-sensitive transcription factors such as NF-κB [31]. Overexpression of Cu/Zn-SOD and catalase in vascular smooth muscle cells has been shown to inhibit VCAM-1 expression through inhibition of NF-κB [31].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of antioxidant enzymes in ApoE-deficient mice suppresses Benzo(a)pyrene-accelerated atherosclerosis

et al. 2009

View full text Add to dashboard Cite

show abstract

“…Thereby the redox state of a cell can be monitored and modulated by gene expression regulation. Indeed, GPx4 has previously been shown to modulate the activity of transcription factors including nuclear factor κB (NF-κB) and Nrf2 (Brigelius-Flohe et al, 1997; Banning et al, 2004; Wenk et al, 2004; Banning and Brigelius-Flohe, 2005). By dampening NF-κB signaling GPx4 reduces expression of matrix metalloproteinase-1 (MMP-1), a protein frequently upregulated during invasion and metastasis of various tumors (Wenk et al, 2004).…”

Section: Selenium-dependent Glutathione Peroxidases and Developmentmentioning

confidence: 99%

The roles of glutathione peroxidases during embryo development

Ufer

Wang

2011

Front. Mol. Neurosci.

104

View full text Add to dashboard Cite

Embryo development relies on the complex interplay of the basic cellular processes including proliferation, differentiation, and apoptotic cell death. Precise regulation of these events is the basis for the establishment of embryonic structures and the organ development. Beginning with fertilization of the oocyte until delivery the developing embryo encounters changing environmental conditions such as varying levels of oxygen, which can give rise to reactive oxygen species (ROS). These challenges are met by the embryo with metabolic adaptations and by an array of anti-oxidative mechanisms. ROS can be deleterious by modifying biological molecules including lipids, proteins, and nucleic acids and may induce abnormal development or even embryonic lethality. On the other hand ROS are vital players of various signaling cascades that affect the balance between cell growth, differentiation, and death. An imbalance or dysregulation of these biological processes may generate cells with abnormal growth and is therefore potentially teratogenic and tumorigenic. Thus, a precise balance between processes generating ROS and those decomposing ROS is critical for normal embryo development. One tier of the cellular protective system against ROS constitutes the family of selenium-dependent glutathione peroxidases (GPx). These enzymes reduce hydroperoxides to the corresponding alcohols at the expense of reduced glutathione. Of special interest within this protein family is the moonlighting enzyme glutathione peroxidase 4 (Gpx4). This enzyme is a scavenger of lipophilic hydroperoxides on one hand, but on the other hand can be transformed into an enzymatically inactive cellular structural component. GPx4 deficiency – in contrast to all other GPx family members – leads to abnormal embryo development and finally produces a lethal phenotype in mice. This review is aimed at summarizing the current knowledge on GPx isoforms during embryo development and tumor development with an emphasis on GPx4.

show abstract

“…TNFα is a known inducer of adhesion molecules like vascular cell adhesion molecule 1 (VCAM1) and intercellular adhesion molecule 1, which are required for monocyte adhesion to endothelial cells and subsequent tissue penetration, a process counteracted by selenium supplementation [16]. In addition, VCAM1 expression is decreased in cells overexpressing the selenoprotein GPx4 [17]. The increase in LPS-induced PGE 2 production depends on cyclooxygenase 2 (COX-2), which is down-regulated by selenium supply [14] and GPx2 [18].…”

Section: Introductionmentioning

confidence: 99%

Marginal selenium deficiency down-regulates inflammation-related genes in splenic leukocytes of the mouse

Kipp

Banning

Schothorst

et al. 2012

The Journal of Nutritional Biochemistry

View full text Add to dashboard Cite

Moderate selenium deficiency may lead to an impaired capacity to cope with health challenges. Functional effects of suboptimal selenium intake are not fully known, and biomarkers for an insufficient selenium supply are inadequate. We therefore fed mice diets of moderately deficient or adequate selenium intake for 6 weeks. Changes in global gene expression were monitored by microarray analysis in splenic leukocytes. Genes for four selenoproteins, Sepw1, Gpx1, Selh and Sep15, were the most significantly down-regulated in moderate selenium deficiency, and this was confirmed by quantitative polymerase chain reaction (qPCR). Classification of significantly affected genes revealed that processes related to inflammation, heme biosynthesis, DNA replication and transcription, cell cycle and transport were affected by selenium restriction. Down-regulation by moderate selenium deficiency of specific genes involved in inflammation and heme biosynthesis was confirmed by qPCR. Myeloperoxidase and lysozyme activities were decreased in selenium-restricted leukocytes, providing evidence for functional consequences. Genes for 31 nuclear factor (NF)-κB targets were down-regulated in moderate selenium deficiency, indicating an impaired NF-κB signaling. Together, the observed changes point to a disturbance in inflammatory response. The selenoproteins found here to be sensitive to selenium intake in murine leukocytes might also be useful as biomarkers for a moderate selenium deficiency in humans.

show abstract

Inhibition of basal and interleukin-1-induced VCAM-1 expression by phospholipid hydroperoxide glutathione peroxidase and 15-lipoxygenase in rabbit aortic smooth muscle cells

Cited by 33 publications

References 57 publications

Overexpression of antioxidant enzymes in ApoE-deficient mice suppresses Benzo(a)pyrene-accelerated atherosclerosis

Overexpression of antioxidant enzymes in ApoE-deficient mice suppresses Benzo(a)pyrene-accelerated atherosclerosis

The roles of glutathione peroxidases during embryo development

Marginal selenium deficiency down-regulates inflammation-related genes in splenic leukocytes of the mouse

Contact Info

Product

Resources

About