Involvement of estrogen-related receptor-γ and mitochondrial content in intrauterine growth restriction and preeclampsia

Poidatz, Dorothée; Santos, Esther Dos; Duval, Fabien; Moindjie, Hadia; Sérazin, Valérie; Vialard, François; Mazancourt, Philippe de; Dieudonné, Marie‐Noëlle

doi:10.1016/j.fertnstert.2015.05.005

Cited by 51 publications

(33 citation statements)

References 48 publications

(69 reference statements)

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“…BPA has been shown to activate estrogen receptors (39), producing effects similar to those induced by natural estrogens (40,41). A relationship between estrogen receptors and metabolites and preeclampsia has been described, but little is known about the contribution of these estrogen receptors or estrogen metabolites to preeclampsia mediated by BPA exposure (42)(43)(44)(45). It has been demonstrated that women with preeclampsia have lower estrogen and disrupted estrogen profiles (43); we speculate, therefore, that it is unlikely that this estrogen disruption is the underlying mechanism in BPA-induced preeclampsia.…”

Section: Discussionmentioning

confidence: 99%

Bisphenol A exposure alters placentation and causes preeclampsia‐like features in pregnant mice involved in reprogramming of DNA methylation ofWNT2

Tang

Xiong

et al. 2018

FASEB j.

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Preeclampsia leads to adverse outcomes for pregnant women. Bisphenol A (BPA) is an environmental endocrine disruptor and has been shown to be positively associated with increased risk of preeclampsia in human studies. We investigated whether BPA exposure causes preeclampsia‐like features in pregnant mice and the associated underlying mechanisms. Experiments were performed in animal models and cell cultures. In pregnant mice, BPA‐exposed mice exhibited preeclampsia‐like features including hypertension, disruption of the circulation, and the placental angiogenesis biomarkers fms‐related tyrosine kinase 1 and placenta growth factor, and glomerular atrophy; urinary protein was not affected. These preeclampsia‐like features correlated with increased retention of smooth muscle cells and reduced vessel areas at the junctional zone of the placenta. In addition, there were disrupted expression of invasion‐related genes including increased tissue inhibitors of metalloproteinases, decreased metalloproteinases, and Wnt family member WJVT2/β‐catenin, which correlated with increased DNA methylation in its promoter region and upregulation of DNA methyltransferase (Dnmt)l. BPA exposure impeded the interaction between the human cytotrophoblast cell line, HTR‐8/SVneo, and endothelium cells. BPA exposure down‐regulated WNT2 expression, and elevated the DNA methylation of WNT2; these results were consistent with in vivo observations. Inhibition of DNMT in HTR‐8/SVneo cells resulted in reduced DNA methylation and increased expression of WNT2. Taken together, these data demonstrate that BPA exposure alters trophoblast cell invasion and causes abnormal placental vessel remodeling, both of which lead to the development of preeclampsia‐like features in pregnant mice. Our results suggest that this phenomenon involves the epigenetic reprogramming and down‐regulation of WNT2 mediated by DNMT1.—Ye, Y., Tang, Y., Xiong, Y., Feng, L., Li, X. Bisphenol A exposure alters placentation and causes preeclampsia‐like features in pregnant mice involved in reprogramming of DNA methylation of WNT2. FASEB J. 33,2732–2742 (2019). http://www.fasebj.org

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Section: Discussionmentioning

confidence: 99%

Bisphenol A exposure alters placentation and causes preeclampsia‐like features in pregnant mice involved in reprogramming of DNA methylation ofWNT2

Tang

Xiong

et al. 2018

FASEB j.

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“…Our SEM results, showing IGF-1 had a direct positive association with levels of mtDNA coding for MT-CO1 and MT-CO2 , contributes to accumulating evidence that mitochondria play a central role in fetal metabolic programming [73]. While this paper was under revision, two manuscripts were published providing more evidence of the dynamic relationship between prenatal exposure, mtDNA content, IUGR and metabolic programing in utero [74]. Effective fetal growth is dependent on the transport of nutrients from the placenta to the fetus, which requires ATP, insulin, and several growth factors, including IGF-1 .…”

Section: Discussionmentioning

confidence: 65%

Prenatal exposure to tobacco smoke leads to increased mitochondrial DNA content in umbilical cord serum associated to reduced gestational age

Pirini

Goldman

Soudry

et al. 2016

International Journal of Environmental Health Research

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We investigated if prenatal exposures to tobacco smoke leads to changes in mitochondrial DNA content (mtDNA) in cord serum and adversely affect newborns health. Umbilical cord serum cotinine levels were used to determine in-utero exposure to smoking. Cord serum mtDNA was measured by quantitative PCR analysis of the genes coding for cytochrome c oxidase1 (MT-CO1) and cytochrome c oxidase2 (MT-CO2). Log transformed levels of mtDNA coding for MT-CO1 and MT-CO2 were significantly higher among infants of active smokers with higher serum level of cotinine (p<0.05) and inversely associated with gestational age (p=0.08; p=0.02). Structural equation modeling results confirmed a positive association between cotinine and MT-CO1 and2 (p<0.01) and inverse associations with gestational age (p=0.02) and IGF-1 (p<0.01). We identified a dose-dependent increase in the level of MT-CO1 and MT-CO2 associated to increases cord serum cotinine and decreased gestational age.

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“…The MB and OP genes were selected from previously published studies based on hypothesized functional and biologic significance and known associations with phenotypes that are related to placental function and/or perinatal outcomes in mammals. 16,28,39–43 …”

Section: Methodsmentioning

confidence: 99%

Abruptio placentae risk and genetic variations in mitochondrial biogenesis and oxidative phosphorylation: replication of a candidate gene association study

Workalemahu

Enquobahrie

Gelaye

et al. 2018

American Journal of Obstetrics and Gynecology

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In this study, we replicated previous findings and provide strong evidence for DNA variants that encode for genes that are involved in mitochondrial biogenesis and oxidative phosphorylation pathways, which confers risk for abruptio placentae. These results shed light on the mechanisms that implicate DNA variants that encode for proteins in mitochondrial function that are responsible for abruptio placentae risk. Therapeutic efforts to reduce risk of abruptio placentae can be enhanced by improved biologic understanding of maternal mitochondrial biogenesis/oxidative phosphorylation pathways and identification of women who would be at high risk for abruptio placentae.

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Involvement of estrogen-related receptor-γ and mitochondrial content in intrauterine growth restriction and preeclampsia

Cited by 51 publications

References 48 publications

Bisphenol A exposure alters placentation and causes preeclampsia‐like features in pregnant mice involved in reprogramming of DNA methylation ofWNT2

Bisphenol A exposure alters placentation and causes preeclampsia‐like features in pregnant mice involved in reprogramming of DNA methylation ofWNT2

Prenatal exposure to tobacco smoke leads to increased mitochondrial DNA content in umbilical cord serum associated to reduced gestational age

Abruptio placentae risk and genetic variations in mitochondrial biogenesis and oxidative phosphorylation: replication of a candidate gene association study

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