Increased 15-HPETE production decreases prostacyclin synthase activity during oxidant stress in aortic endothelial cells

Weaver, James; Maddox, Jane F.; Cao, Yu-Zhang; Mullarky, Isis K.; Sordillo, Lorraine M.

doi:10.1016/s0891-5849(00)00466-4

Cited by 49 publications

(31 citation statements)

References 17 publications

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“…Glutathione peroxidase activity of -Se BMEC was significantly lower (P < 0.05) than the activity levels of +Se BMECs (Table 1). These values are similar to those observed in other studies using ECs and represent differences that occur in vivo in Se-sufficient and -deficient animals (38,41,42). To examine the effect of Se status and altered selenoprotein activity on VEGF production, TrxR activity was chemically inhibited by the use of DNCB.…”

Section: Vegf Protein Production Following Trxr Inhibitionsupporting

confidence: 86%

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Thioredoxin Reductase Regulates Angiogenesis by Increasing Endothelial Cell-Derived Vascular Endothelial Growth Factor

Streicher

Sylte²,

Johnson³

et al. 2004

Nutrition and Cancer

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Low selenium (Se) status increases angiogenesis by inducing the production of vascular endothelial growth factor (VEGF); however, the mechanism responsible for VEGF up-regulation has yet to be characterized. Se's ability to control cellular oxidative state through its incorporation into selenoproteins such as thioredoxin reductase (TrxR) may explain previous studies that connect Se status to tumor angiogenesis. Therefore, the focus of this study was to determine if altered VEGF expression and angiogenesis due to decreased Se levels are influenced by reduced TrxR activity. We found that chemical inhibition of TrxR in Se-sufficient endothelial cells (ECs) was associated with increases in VEGF and VEGF receptor expression, cell migration, proliferation, and angiogenesis to levels similar to those seen in Se-deficient ECs. Specific inhibition of glutathione peroxidase did not affect pro-angiogenic responses, indicating a unique role of the TrxR system during low Se status. These data correlate changes in TrxR activity with changes in VEGF expression and angiogenic development in ECs, which is significant because minimal mechanistic data exist that explain the role of Se in cancer prevention. Understanding the importance of the tumor microenvironment in contributing to angiogenic regulation has the potential to significantly impact breast cancer chemoprevention strategies by focusing on maintaining proper EC function within the mammary gland.

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Section: Vegf Protein Production Following Trxr Inhibitionsupporting

confidence: 86%

“…Total RNA was isolated from BMECs with TRIZOL® Reagent (Invitrogen) according to the manufacturer's instructions, and 100 ng was used in all reactions. Quantitative, competitive RT-PCR was performed as previously described (41).…”

Section: Quantitative Competitive Reverse Transcription-polymerase Chmentioning

confidence: 99%

Thioredoxin Reductase Regulates Angiogenesis by Increasing Endothelial Cell-Derived Vascular Endothelial Growth Factor

Streicher

Sylte²,

Johnson³

et al. 2004

Nutrition and Cancer

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“…Se-deficient bovine aortic endothelial cells cultured in the presence of only 0·01 ppm Se were characterised by a significant decrease in GPx1 activity with concomitant increases in 15-HPETE and TXB 2 compared with cells supplemented with 10 ng/ml sodium selenite ( 91 ) . The same group then explored the association between diminished Se status of endothelial cells and the ability of 15-HPETE to elicit signs of oxidative stress ( 36 ) , enhanced adhesion molecule expression ( 92 ) , higher rates of apoptosis ( 93 ) and dampened expression of PGI 2 ( 94 ) . Collectively, these studies support the concept that the antioxidant ability of selenoproteins is necessary to mitigate the pro-inflammatory effects of 15-HPETE and reduce endothelial cell death as a consequence of oxidative stress.…”

Section: Can Selemium and Selenoproteins Have An Impact On Inflammatimentioning

confidence: 99%

Regulation of inflammation by selenium and selenoproteins: impact on eicosanoid biosynthesis

2013

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Uncontrolled inflammation is a contributing factor to many leading causes of human morbidity and mortality including atherosclerosis, cancer and diabetes. Se is an essential nutrient in the mammalian diet that has some anti-inflammatory properties and, at sufficient amounts in the diet, has been shown to be protective in various inflammatory-based disease models. More recently, Se has been shown to alter the expression of eicosanoids that orchestrate the initiation, magnitude and resolution of inflammation. Many of the health benefits of Se are thought to be due to antioxidant and redox-regulating properties of certain selenoproteins. The present review will discuss the existing evidence that supports the concept that optimal Se intake can mitigate dysfunctional inflammatory responses, in part, through the regulation of eicosanoid metabolism. The ability of selenoproteins to alter the biosynthesis of eicosanoids by reducing oxidative stress and/or by modifying redox-regulated signalling pathways also will be discussed. Based on the current literature, however, it is clear that more research is necessary to uncover the specific beneficial mechanisms behind the anti-inflammatory properties of selenoproteins and other Se metabolites, especially as related to eicosanoid biosynthesis. A better understanding of the mechanisms involved in Se-mediated regulation of host inflammatory responses may lead to the development of dietary intervention strategies that take optimal advantage of its biological potency.

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“…Selenium is an essential trace element with an antioxidant property and may play a role in the clinical severity of CHF [180]. Selenium depleted states have glutathione peroxidase deficiency (antioxidant) and increased 15-hydroperoxyeicosatetraenoic acid with consequent decreased endothelial prostacyclin synthase activity [181,182].…”

Section: Importance Of Ethnic Specific Nutrient Factorsmentioning

confidence: 99%

Endothelial dysfunction in African-Americans

Patel

Velazquez

Arora

2009

International Journal of Cardiology

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Increased 15-HPETE production decreases prostacyclin synthase activity during oxidant stress in aortic endothelial cells

Cited by 49 publications

References 17 publications

Thioredoxin Reductase Regulates Angiogenesis by Increasing Endothelial Cell-Derived Vascular Endothelial Growth Factor

Thioredoxin Reductase Regulates Angiogenesis by Increasing Endothelial Cell-Derived Vascular Endothelial Growth Factor

Regulation of inflammation by selenium and selenoproteins: impact on eicosanoid biosynthesis

Endothelial dysfunction in African-Americans

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