Selenium deficiency inhibits prostacyclin release and enhances production of platelet activating factor by human endothelial cells

Hampel, G; Watanabe, Kentaro; Weksler, Babette B.; Jaffe, Eric

doi:10.1016/0005-2760(89)90189-6

Cited by 53 publications

(16 citation statements)

References 66 publications

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“…33,34) It was reported that Se deficiency inhibited prostacyclin release by human endothelial cells. 55) Se deficiency might cause an imbalance between the production of thromboxane A 2 -like lipids including 8-isoprostane and prostacyclin. The imbalance might contribute both to the progression of atherosclerosis and to increased vascular occlussion in patients with coronary artery disease, resulting in the increased incidence of myocardial infarction and other atherosclerotic cardiovascular diseases associated with low serum Se levels.…”

Section: Discussionmentioning

confidence: 99%

Effects of Selenium Deficiency on Expression of Selenoproteins in Bovine Arterial Endothelial Cells.

Hara

Shoji

Sakurai

et al. 2001

Biological & Pharmaceutical Bulletin

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Selenium (Se) is an essential trace element and functions primarily in the form of selenoproteins. [1][2][3][4][5] Se is incorporated into selenoproteins in the form of selenocysteine, and its incorporation is directed by a specific UGA codon, which normally functions as a stop codon in both prokaryocytes and eukaryocytes. 6) In mammals, 14 selenoproteins have been found to date.2,3) These include four types of glutathione peroxidase (GPx), 7) three types of thyroid hormone deiodinase, 8) three types of thioredoxin reductase (TrxR), 9,10) selenophosphate synthetase 2, 11) selenoprotein W, 12) selenoprotein P (SelP), 13) and the 15-kDa selenoprotein. 14) In addition to these selenoproteins, a computational screening identified three other new mammalian selenoproteins. 15,16) Se deficiency causes a fall in the activities and mRNA levels of selenoproteins. 4,5) In humans, severe Se deficiency is associated with cardiac disease (Keshan disease) in some provinces of China. 5,17) It has also been reported that deficiency of Se is associated with an increased incidence of myocardial infarction and other atherosclerotic cardiovascular diseases. 18,19) Reactive oxygen species (ROS) have been implicated in the pathogenesis of many cardiovascular diseases including atherosclerosis.20) The vascular endothelium represents a critical cell target in these disorders. ROS stimulate endothelial lipid peroxidation, 21) perturb the barrier function of vascular endothelial cells (EC), 22) and then interfere with endothelial functions. Selenoproteins such as GPx isozymes, TrxR isozymes and SelP have an activity to scavenge ROS and lipid peroxides. 23,24) Thomas et al. found that Se supplementation confers resistance on EC to oxidative injury.25) The possible mechanism for this protection is considered to be through the expression of selenoproteins. However, the expression and the regulation of selenoproteins in vascular EC have not yet been well understood.In the present study, we detected the expression of several selenoproteins including TrxR isozymes, GPx isozymes and SelP in cultured bovine arterial EC (BAEC) and then investigated the effect of Se depletion on the expression of these selenoproteins. MATERIALS AND METHODSCell Culture BAEC were kindly provided by Dr. M. Masuda of the National Cardiovascular Research Institute (Osaka, Japan). BAEC were cultured and maintained in Dulbecco's modified Eagle's medium (DMEM) containing 10% fetal calf serum (FCS). In order to prepare Se-sufficient and Se-deficient cells, the cells were grown in 0.5% FCS-containing DMEM supplemented either with insulin (5 mg/ml), transferrin (0.5 mg/ml) and sodium selenite (100 nM) (Se-sufficient medium) or with insulin and transferrin (Se-deficient medium) alone.Measurement of Sensitivity of BAEC to tert-Butylhydroperoxide (t-BuOOH) The sensitivity of BAEC to tBuOOH was determined by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay as described previously.26) BAEC cultured in Se-deficient or Se-sufficient medium for 6 d were resu...

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Section: Discussionmentioning

confidence: 99%

Effects of Selenium Deficiency on Expression of Selenoproteins in Bovine Arterial Endothelial Cells.

Hara

Shoji

Sakurai

et al. 2001

Biological & Pharmaceutical Bulletin

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“…Further, endothelial cells of various kinds express different levels of peroxidases involved in protecting endothelial cells against oxidative stress [42]. For instance, glutathione peroxidase levels in bovine aortic endothelial cells are significantly lower than in HUVEC [43]. Since (a) the adhesion of monocytes is an early event in lesion formation, (b) oxidized LDL increase monocyte adhesion to endothelial cells, (c) oxidation renders LDL more atherogenic [lo] and (d) epidemiological and experimental studies have shown that HDL are protective against atherosclerosis [21], we questioned whether HDL could modulate oxidized LDL induction of U937 adhesion to endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

The protective role of high‐density lipoprotein on oxidized‐low‐density‐lipoprotein‐induced U937/endothelial cell interactions

Maier

Barenghi²,

Pagani³

et al. 1994

European Journal of Biochemistry

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The adherence of monocytes to the endothelium is an early event in atherogenesis. We have investigated this process by examining whether native and oxidized low-density and high-density lipoproteins could modulate this process. Only oxidized low-density lipoprotein caused a significant dose-dependent and time-dependent increase in U937 monocyte-like cell line binding to human endothelial cells, by a process which required de nova protein synthesis. Interestingly, E-selectin, intercellular adhesion molecule-1, vascular cell-adhesion molecule or P-selectin induction was not apparent in this system suggesting the presence of an alternative system for the interaction of endothelial cells with monocyte-like cells in response to oxidized low-density lipoprotein. Highdensity lipoprotein completely suppressed oxidized low-density-lipoprotein-induced adhesion of U937 cells to the endothelial monolayer, while oxidized high-density lipoprotein did not. These data suggest that the balance between native and oxidized lipoproteins may play a role in the formation of the atherosclerotic lesion by modulating monocyte endothelial interactions.One of the earliest detectable events in human and experimental atherosclerosis is the adherence of circulating monocytes to the arterial endothelial lining [l]. Monocyte recruitment may involve changes in endothelial adhesiveness for monocytes [2] and the local production of monocyte chemotactic molecules [3]. Several molecules that are inducible on the endothelial surface and can support the adhesion of monocytes have been identified [4 -71. Indeed, these molecules could be involved in the recruitment of monocytes in atherosclerosis, since intercellular adhesion molecule-1 (ICAM-1) and E-selectin are expressed in human atherosclerotic lesions in vivo [8] [3] and increase the levels of monocyte colony-stimulating factor (M-CSF) which may promote macrophage differentiation [ 171. Although heterogeneous oxidized LDL are present in the blood [18], in the artery wall [19] and in atherosclerotic lesions [20], no data are available about the modulation of endothelial behavior by LDL which have been oxidized to various extents.Epidemiological evidence establishes an inverse correlation between the levels of plasma high-density-lipoprotein cholesterol and atherosclerosis [211. However, the biochemical mechanism(s) of action of high-density lipoproteins (HDL) in preventing the development of atherosclerotic lesions are not established. The most widely accepted hypothesis is that HDL facilitate the clearance of cholesterol from the atheromatous plaques and its transport to the liver for excretion [21]. In addition, HDL have been reported to play a protective role in atherogenesis by preventing the generation of oxidatively modified LDL [22, 231. Interestingly, HDL oxidation can occur in vitro 124, 251 and in vivo [26], and oxidized HDL have been shown to possess a broad range of biological activities [27-301. In this study, we investigate the effects of mildly and extensively oxidized LDL on the adh...

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“…A dietary deficiency of Se has been incriminated in the etiology of cardiovascular diseases and Se supplementation can protect human endothelial cells from oxidative injury [10]. Dietary Se may be considered anti-atherosclerotic [11]. Previous reports and our early investigations suggest that an inverse relationship exists between dietary Se and antioxidant capacity of rat cardiovascular tissues [12,13] and in the status of Se deficient, 3-triol injured arterial endothelium more severely than that in the status of Se adequate [14].…”

Section: Introductionmentioning

confidence: 96%

Inhibiting effect of selenium on oxysterols-induced apoptosis of rat vascular smooth muscle cells

Tang

Huang

2004

Journal of Inorganic Biochemistry

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Selenium deficiency inhibits prostacyclin release and enhances production of platelet activating factor by human endothelial cells

Cited by 53 publications

References 66 publications

Effects of Selenium Deficiency on Expression of Selenoproteins in Bovine Arterial Endothelial Cells.

Effects of Selenium Deficiency on Expression of Selenoproteins in Bovine Arterial Endothelial Cells.

The protective role of high‐density lipoprotein on oxidized‐low‐density‐lipoprotein‐induced U937/endothelial cell interactions

Inhibiting effect of selenium on oxysterols-induced apoptosis of rat vascular smooth muscle cells

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