1,25(OH)2D3 suppresses COX-2 up-regulation and thromboxane production in placental trophoblast cells in response to hypoxic stimulation

Sun, Jian; Zhong, Weijie; Gu, Yang; Groome, Lynn J.; Wang, Yuping

doi:10.1016/j.placenta.2013.12.002

Cited by 27 publications

(13 citation statements)

References 29 publications

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“…In keeping with this action to enhance antioxidant pathways, vitamin D increased the ratio of intracellular reduced to oxidized glutathione and decreased the production of 8-isoprostane. This action of vitamin D is consistent with previous evidence that it can protect various other types of epithelial cell from oxidative stress in vitro , including H 2 O 2 -treated prostatic and breast epithelial cells [51] [52] and CoCl 2 -treated trophoblasts [53]. Similarly, using immortalised epithelial cell lines, notwithstanding that immortalised cell lines are known to manifest distinctly different responses to vitamin D [54], it has been shown that vitamin D can abrogate impairment caused by oxidative stress of nuclear translocation of the ligand bound glucocorticoid receptor [55].…”

Section: Discussionsupporting

confidence: 90%

Effects of vitamin D on inflammatory and oxidative stress responses of human bronchial epithelial cells exposed to particulate matter

Pfeffer

Mann

et al. 2018

Preprint

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41 Background: Particulate matter (PM) pollutant exposure, which induces oxidative stress and 42 inflammation, and vitamin D insufficiency, which compromises immune regulation, are 43 detrimental in asthma. 55 versus asthmatic donor cultures. Vitamin D also differentially affected PM-stimulated GM-56 CSF, with suppression in healthy HBECs and enhancement in asthmatic cultures. Vitamin D 57 increased HBEC expression of the antioxidant pathway gene G6PD, increased the ratio of 58 reduced to oxidised glutathione, and in PM-stimulated cultures decreased the formation of 8-59 isoprostane. Pre-treatment with vitamin D decreased CXCL8 and further decreased IL-6 60 production in PM-stimulated cultures, an effect abrogated by inhibition of G6PD with DHEA, 61 supporting a role for this pathway in the anti-inflammatory actions of vitamin D. 62 Conclusions: In a study using HBECs from 18 donors, vitamin D enhanced HBEC 63 antioxidant responses and modulated the immune response to PM, suggesting that vitamin D 64 may protect the airways from pathological pollution-induced inflammation. prevalence, implying the importance of environmental factors in its aetiology [1]. Vitamin D 68 insufficiency/deficiency and ambient air pollution are two major environmental factors that 69 appear to influence the pathogenesis and stability of asthma [2] [3] [4] [5], as well as other 70 respiratory diseases [6] [7]. However there remains debate resulting from the heterogeneity 71 of findings relating to the effects of these environmental factors on airway pathology [5] [8] [9] 72 [10]. For example, European studies have shown heterogeneity between different cities in 73 the magnitude of the effects of pollution on health outcomes such as hospital admissions for 74 respiratory diseases [9] and asthma incidence [11], despite using standardised analyses. 75 Environment-environment interactions are a major possible explanation for inconsistent 76 results between different patient cohorts but have been little studied, particularly at the 77 mechanistic level. In a recent meta-analysis, latitude of study location influenced 78 associations between air pollutants and severe asthma exacerbations, and latitude is also 79 known to affect sunlight-derived vitamin D production, although this association is 80 complicated by other factors such as hours of daily skin exposure to sunlight [5]. In the 81 urban environment Rosser and colleagues have shown that vitamin D insufficient children, 82 but not those vitamin D sufficient, living close to major roads show an elevated risk of severe 83 asthma exacerbations [12], although the mechanisms by which vitamin D may protect 84 against pollution toxicity remain unclear and the interaction likely complex. 85 86 A growing body of research highlights the importance of epithelial immunology in 87 asthma [13]. Evidence shows that inhaled ambient particulate matter (PM) adversely affects 88 the bronchial epithelium through various mechanisms including the imposition of oxidative 89 stress, which stimulates redox sensi...

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Section: Discussionsupporting

confidence: 90%

Effects of vitamin D on inflammatory and oxidative stress responses of human bronchial epithelial cells exposed to particulate matter

Pfeffer

Mann

et al. 2018

Preprint

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“…Our study showed that aspirin probably inhibits the production of sFlt1 by the COX-1 pathway. Our study also showed that, hypoxia did not change COX1 and COX2 mRNA expression although some have reported that the hypoxia mimic, CoCl 2 increases COX2 but not COX1 in trophoblasts and others have reported that hypoxia reoxygenation increases COX-1 and COX-2 expression in murine placental explants (44, 45). We found that both aspirin and sc-560 decreased COX1 mRNA expression while increasing COX2 mRNA expression.…”

Section: Discussionsupporting

confidence: 48%

Aspirin inhibits expression of sFLT1 from human cytotrophoblasts induced by hypoxia, via cyclo-oxygenase 1

Li¹,

Raikwar

Santillan³

et al. 2015

Placenta

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Introduction Elevated circulating soluble FLT1 (sFLT1) levels in preeclampsia may play a role in its development. Aspirin is recommended for prevention of preeclampsia. We hypothesized that aspirin may inhibit the production of sFlt1. Methods Placentas from women with and without preeclampsia were collected. Primary cytotrophoblasts (CTBs) were cultured from normal placentas and treated with aspirin, sc-560, a COX1 inhibitor or celecoxib, a COX-2 inhibitor. The expression of sFLT1, FLT1, COX1, COX2 was studied. The effect of aspirin on sFlt1 expression was also studied in HEK293 cells and in HTR-8/SVNeo cells. Results The expression of sFLT1 was increased in preeclamptic placentas compared to control placentas and the expression and release of sFLT1 increased in CTBs exposed to 2% O2 compared to controls. Aspirin at 3 and 12 mM concentration reduced the expression and release of sFLT1 in CTBs. Aspirin also inhibited sFlt1 expression from HTR-8/SVNeo and HEK293 cells. Sc-560, but not celecoxib, reduced sFLT1 expression and release from CTBs. Aspirin and sc-560 also reduced hypoxia-induced FLT1 mRNA expression and inhibited COX1 mRNA in CTBs. Discussion This study confirms that sFLT1 expression is increased in preeclamptic placentas and in CTBs exposed to hypoxia. Aspirin inhibits the production sFLT1 in CTBs and in HTR-8/SVNeo. Sc-560 recapitulated the effects of aspirin on sFLT1 expression and release in CTBs suggesting that the aspirin effect may be mediated via inhibition of COX1. The study increases our understanding of the mechanisms regulating sFlt1 expression and provides a plausible explanation for the effect of aspirin to prevent preeclampsia.

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“…Although it is not clear whether the VDR binds directly to the promoter of MMP2 and MMP9 genes, due to the available binding site of NFkB on the promotor of the MMP2 and MMP9 genes (Zhang et al, ; Andrés, ), it seems that reduction in MMPs expression may be done through NFkB deactivation. Anyway, reduced synthesis of proinflammatory cytokines such as IL‐6 and TNF‐α by monocytes (Zhang et al, ), reduced synthesis of adhesion molecule, c‐reactive protein (Brewer et al, ), COX‐1 (Sun et al, ), and phagocytic receptors such as CD36 (Oh et al, ) are observed under the influence of vitamin D. Despite these anti‐atherogenic effects, it is observed that 1,25‐dihydroxyvitamin D3 induces VSMC migration via activation of phosphatidylinositol 3‐kinase (Rebsamen et al, ).…”

Section: Vitamin Effects On Atherosclerosismentioning

confidence: 99%

Anti‐Atherosclerotic Effects of Vitamins D and E in Suppression of Atherogenesis

Rashidi

Hoseini

Sahebkar

et al. 2017

Journal Cellular Physiology

104

107

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Atherosclerosis is a progressive and multifactorial disease which occurs under the influence of various risk factors including endothelial dysfunction (ED), oxidative stress, and low-density lipoprotein (LDL) oxidation. In contract to the initial hypotheses on the usefulness of vitamin E supplementation for cardiovascular disease prevention, large outcome trials showed consumption of vitamin E has no obvious effect on cardiovascular disease and, in some cases, it may even increase the rate of mortality. This seemingly unexpected finding may be due to the opposite effects of vitamin E compounds. Vitamin E is a group of compounds which have different and even opposing effects, yet in most of the studies, the exact consumed component of vitamin E is not determined. It appears that the combined consumption of gamma-tocopherol, vitamin C, D, and tetrahydrobiopterin (BH4) may be extremely effective in both preventing atherogenesis and suppressing plaque development. In this regard, one of main issues is effect of vitamins E and D deficiency on microRNAs network in atherosclerosis. Various studies have indicated that miRNAs have key roles in atherosclerosis pathogenesis. The deficiency of vitamins E and D could provide a deregulation for miRNAs network and these events could lead to progression of atherosclerosis. Here, we highlighted a variety of mechanisms involve in the progression of atherosclerosis and effects of vitamins D and E on these mechanisms. Moreover, we summarized miRNAs involve in atherosclerosis and their regulation by vitamins E and D deficiency. J. Cell. Physiol. 232: 2968-2976, 2017. © 2016 Wiley Periodicals, Inc.

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1,25(OH)2D3 suppresses COX-2 up-regulation and thromboxane production in placental trophoblast cells in response to hypoxic stimulation

Cited by 27 publications

References 29 publications

Effects of vitamin D on inflammatory and oxidative stress responses of human bronchial epithelial cells exposed to particulate matter

Effects of vitamin D on inflammatory and oxidative stress responses of human bronchial epithelial cells exposed to particulate matter

Aspirin inhibits expression of sFLT1 from human cytotrophoblasts induced by hypoxia, via cyclo-oxygenase 1

Anti‐Atherosclerotic Effects of Vitamins D and E in Suppression of Atherogenesis

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