Angiogenesis in the Placenta: The Role of Reactive Oxygen Species Signaling

Pereira, Robyn D.; Long, Nicole E. De; Wang, Ruijun C.; Yazdi, Fereshteh; Holloway, Alison C.; Raha, Sandeep

doi:10.1155/2015/814543

Cited by 166 publications

(134 citation statements)

References 137 publications

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“…30 Transcription factors that take part in vascular development include E26 transformation-specific oncogene homolog-1 (Ets-1), Kr€ uppel-like factor-8 (KLF-8), Nrf-2, specificity protein-1 (Sp-1), Sp-3 and signal transducer and activator of transcription-3 (STAT-3). 31 Some researchers have focused on the promising therapeutic significance of Nrf-2 in PE for its cytoprotective effects. 32 In response to OS, Nrf-2 dissociates from its repressor and binds to a gene promoter region of various genes.…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress: Placenta Function and Dysfunction

Tian

Lin

et al. 2015

American J Rep Immunol

143

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During pregnancy, the placenta is a site of active oxygen metabolism that continuously generates oxidative stress (OS). Overproduction of reactive oxygen species and reactive nitrogen species can destroy normal placental functions. Therefore, the feto-placental unit generates abundant antioxidants to keep OS under control. Properly controlled oxidative species have been proven to serve as indispensable cellular signal messengers by regulating gene expression and downstream cellular activities. OS also plays an important immunoregulatory role during pregnancy. Oxidative disorder and immune disturbances are associated with adverse pregnancy outcomes such as spontaneous abortion, preeclampsia and intrauterine growth restriction. In this review, we introduce recent studies revealing basal functions and regulatory roles of placental OS in metabolism and immunity. The relationships between OS- and pregnancy-related disorders are also discussed.

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Section: Introductionmentioning

confidence: 99%

Oxidative Stress: Placenta Function and Dysfunction

Tian

Lin

et al. 2015

American J Rep Immunol

143

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“…Such factors may contribute to decreased fetal nutrition and oxygenation through oxidative stress that may lead to microvascular endothelial dysfunction and/or disturbed development and function of the placenta, and by reduced blood flow to the placenta due to macrovascular vessel dysfunction from atherosclerosis (Henriksen & Clausen, 2002, Pereira et al, 2015, Reynolds et al, 2006). We suggest that such mechanisms may also explain the unexpected negative association between SSC intake and BW in the non‐GDM pregnancies.…”

Section: Discussionmentioning

confidence: 99%

Is consumption of sugar‐sweetened soft drinks during pregnancy associated with birth weight?

Grundt

Eide

Brantsæter

et al. 2016

Maternal & Child Nutrition

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In Norway, there were parallel increases and subsequent decreases in birth weight (BW) and consumption of sugar‐sweetened carbonated soft drinks (SSC) during the period 1990–2010, and by an ecological approach, we have suggested that the relationship was causal. The objective of this study was to examine if such a relationship was present in a prospectively followed cohort of pregnant women. The study population included 62,494 term singleton mother–infant dyads in the Norwegian Mother and Child Cohort Study (MoBa), a national prospective cohort study in Norway from 1999 to 2008. The association between SSC consumption and BW was assessed using multiple regression analyses with adjustment for potential confounders. Each 100 ml intake of SSC was associated with a 7.8 g (95% confidence interval [CI]: −10.3 to −5.3) decrease in BW, a decreased risk of BW > 4,500 g (odds ratio [OR]: 0.94, 95% CI: 0.90 to 0.97) and a near significantly increased risk of BW < 2,500 g (OR: 1.05, 95% CI: 0.99 to 1.10). The negative association with SSC consumption was aggravated by smoking, lack of exercise, and obesity. For mothers with gestational diabetes mellitus, we observed an increased risk of BW > 4,500 g (OR: 1.18, 95% CI: 1.00 to 1.39) and a trend towards significant increase in mean BW (25.1 g, 95% CI: −2.0 to 52.2) per 100 ml SSC. Our findings suggest that increasing consumption of rapidly absorbed sugar from SSC had opposite associations with BW in normal pregnancies and pregnancies complicated by gestational diabetes mellitus.

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“…Il est bien établi qu'un index de masse corporelle élevé au moment de la grossesse est associé à une altération des marqueurs angiogéniques maternels circulants comme sFlt-1 (soluble fms-like tyrosine kinase-1) et PlGF (placental growth factor) [12,13], reflétant l'existence de désordres de la fonction vasculaire qui touchent à la fois l'endothélium et les cellules musculaires lisses. Ces désordres contribueraient à l'apparition d'une pré-éclampsie, pathologie spécifique de l'espèce humaine caractérisée par un défaut d'invasion et de remodelage des artères spiralées utérines.…”

Section: Obésité Et Vascularisation Placentaireunclassified

Impact de l’obésité et du diabète maternels sur la fonction placentaire

et al. 2016

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> Situé à l'interface foeto-maternelle, le placenta exerce des fonctions d'échanges, endocrines et immunitaires qui influencent le développement foetal. En contact direct avec l'environnement maternel, cet organe est sensible aux désordres métaboliques comme la surnutrition, l'obésité ou le diabète. L'altération des paramètres sanguins associée à ces conditions affecte l'histologie, la vascularisation et les transferts des nutriments placentaires et induit, en fonction du trouble métabolique, une inflammation locale ou une hypoxie. Ces modifications placentaires perturbent le développement et la croissance foetale, ce qui augmente le risque de pathologies à l'âge adulte chez la descendance. Le placenta est donc un acteur incontournable de la programmation foetale. < cet environnement afin d'optimiser le transport des nutriments et des gaz et ainsi promouvoir la survie foetale. Les modifications phénotypiques du placenta ayant des effets sur le phénotype de l'individu, le placenta représente donc un acteur crucial de la programmation foetale ou DOHaD (developmental origins of health and disease), concept développé dans ce numéro thématique de médecine/sciences qui lui est consacré [4]. Dans cette synthèse, nous présenterons notamment l'impact des désordres métaboliques maternels, tels que l'obésité et le diabète, sur la fonction placentaire en nous appuyant sur des données obtenues chez l'homme et à partir de modèles animaux. Effets de l'obésité sur la fonction placentaireLa prévalence de l'obésité ne cesse d'augmenter dans le monde. En France, d'après l'enquête ObEpi-Roche publiée en 2012 1 , une femme sur cinq en âge de procréer est en surpoids, et environ 15 % des femmes présentent une obésité (index de masse corporelle, IMC ≥ 30 kg/m 2 ). Cette obésité pré-gestationnelle favorise, au cours de la grossesse, les anomalies de la croissance foetale, le développement d'un diabète gestationnel, le retard de croissance intra-utérin (RCIU) ou la macrosomie, la pré-éclampsie et la mortalité foetale (➜).1

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Angiogenesis in the Placenta: The Role of Reactive Oxygen Species Signaling

Cited by 166 publications

References 137 publications

Oxidative Stress: Placenta Function and Dysfunction

Oxidative Stress: Placenta Function and Dysfunction

Is consumption of sugar‐sweetened soft drinks during pregnancy associated with birth weight?

Impact de l’obésité et du diabète maternels sur la fonction placentaire

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