NADPH oxidase as an important source of reactive oxygen species at the mouse maternal–fetal interface: putative biological roles

Bevilacqua, Estela; Gomes, Sara Zago; Lorenzon-Ojea, Aline R.; Hoshida, Mara Sandra; Amarante-Paffaro, A. M. Do

doi:10.1016/j.rbmo.2012.03.016

Cited by 25 publications

(17 citation statements)

References 87 publications

(115 reference statements)

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“…They are generated at the maternal-fetal interface at the decidual, trophoblast, and mesenchymal levels. Physiological ROS levels play an important regulatory role through various signaling transduction pathways in uterine function, embryogenesis, embryonic implantation, and feto-placental development [16,31,32]. However, the imbalance between antioxidants and ROS production (oxidative stress) is a causative agent in FGR [11,12,13].…”

Section: Discussionmentioning

confidence: 99%

“…Dysfunctions of several molecules, such as nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, alpha-1-antitrypsin (SERPINA1), insulin-like growth factor (IGF) and vascular endothelial growth factor (VEGF), might correlate with abnormal trophoblast invasion and vascular development, and oxidative stress in the placenta of FGR subjects [16,17,18,19,20,21,22]. The expression levels of apoptosis associated factors, such as ATP-dependent RNA helicase (DDX42), Bcl-2, p53, low-density lipoprotein (LDL), apo B and matrix metalloproteinases, changed during FGR development [6,23,24,25,26,27,28].…”

Section: Introductionmentioning

confidence: 99%

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Comparative Proteomic Profile of the Human Placenta in Normal and Fetal Growth Restriction Subjects

Miao

Chen

Wang

et al. 2014

Cell Physiol Biochem

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Background: Fetal growth restriction (FGR) is the main cause of intrauterine fetal death and the second leading cause of death in the neonatal period. A large body of evidence suggests that FGR may be associated with the placenta, although its etiology and pathogenesis remain to be fully elucidated. Methods and Results: To better understand the molecular mechanisms underlying the pathological development of the placenta in FGR, we used tandem mass tags (TMTs) to construct a large-scale comparative proteomic profile of human placentas from normal and FGR pregnancies. A total of 1,198 kinds of proteins were identified in the control and FGR placentas, of which 95 were differentially expressed between two groups. Ingenuity Pathway Analysis (IPA) was used to organize these differentially expressed proteins into networks of interacting proteins and to identify the modules of functionally related proteins. Western blotting was used to verify the expression patterns of several randomly selected proteins. Conclusion: The placentas of women with FGR displayed significant proteome differences compared with normal pregnancy. The results indicate that a variety of mechanisms and proteins may contribute to the development of FGR. Further studies and validations are required to elucidate the exact roles of these proteins in FGR pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Comparative Proteomic Profile of the Human Placenta in Normal and Fetal Growth Restriction Subjects

Miao

Chen

Wang

et al. 2014

Cell Physiol Biochem

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“…Maternal α-tocopherol supplementation resulted in significantly lower ROS levels in SR-BI −/− embryos, similar to the fluorescence levels in SR-BI +/+ embryos. Trophoblast giant cells have been shown to produce significant ROS due to high activity of the enzyme NADPH oxidase 18 . However, SR-BI deficiency did not affect ROS levels in parietal yolk sacs from embryos obtained from mothers fed control or vitamin E-enriched diets (Fig.…”

Section: Resultsmentioning

confidence: 99%

Deficient Vitamin E Uptake During Development Impairs Neural Tube Closure in Mice Lacking Lipoprotein Receptor SR-BI

Santander

Lizama

Parga

et al. 2017

Sci Rep

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SR-BI is the main receptor for high density lipoproteins (HDL) and mediates the bidirectional transport of lipids, such as cholesterol and vitamin E, between these particles and cells. During early development, SR-BI is expressed in extraembryonic tissueScavenger Receptor Class B type I (SR-BI) is the main receptor for high density lipoproteins (HDL), and numerous studies have described its role in mediating the bidirectional transport of lipids between these lipoproteins and cells 1 . In the liver, SR-BI is involved in the uptake of cholesterol from HDL and its excretion in bile, the final step in reverse cholesterol transport. SR-BI also participates in the uptake of cholesterol in steroidogenic tissues, such as the adrenal glands and ovaries, to be used as a substrate for steroid hormone synthesis 2 . Important information on the roles of SR-BI other than in cholesterol homeostasis and cholesterol provision for steroidogenesis, such as platelet aggregation, erythrocyte maturation and oocyte meiosis, has been generated from the SR-BI knock out (SR-BI −/− ) mouse since it was generated almost two decades ago 3 .In generating SR-BI −/− mice via heterozygous intercrosses, researchers noted that the proportion of weaned homozygous null mice was half that expected by the Mendelian ratio 3 . This evidence, together with the fact that SR-BI is present in murine trophoblasts involved in maternal-foetal nutrient exchange at different stages of gestation 4 , led researchers to postulate that this HDL receptor might be involved in embryonic development. We recently showed that nearly 50% of SR-BI −/− embryos fail to close the anterior neural tube and develop cranial NTD and exencephaly 5 , leading to perinatal death, which explains the deviation from the Mendelian ratio previously reported in weaned SR-BI null mice 3 . Among the spectrum of defective neurulation conditions conferred by abnormal closure at different portions of the neural tube, only cranial NTD is observed in SR-BI −/− embryos.During murine early development, SR-BI is not detected in the embryo itself but rather in trophoblast giant cells (TGC) from the parietal yolk sac 4,5 . TGC play a critical role in embryonic uptake of various nutrients from the maternal blood supply before the establishment of a mature placenta 6 . Despite the prominent role of SR-BI

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“…We next studied cell‐specific NADPHox isoform expression: NOX1, NOX4 (expressed in SMCs), NOX2 (macrophages), and NOX5 (endothelium), all described as being expressed in the myometrium (22, 23). We first performed a screening of these isoforms' expression by RT‐PCR and observed that only NOX2 and NOX4 transcript expression were induced by LPS (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Indeed, O2 •− dimutation leads to hydrogen peroxide (H 2 O 2 ) formation that crosses biologic membranes. Further, the reaction of O2 •− with H 2 O 2 in the presence of transition metals can lead to the formation of the highly cytotoxic hydroxyl radical (OH*), responsible for cell structure and components damages (22, 23). Finally, O2 •− reaction with an excess of • NO can lead to the production of peroxynitrite, a cytotoxic oxidant species, and subsequent nitrosative stress.…”

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confidence: 99%

Glutathione prevents preterm parturition and fetal death by targeting macrophage‐induced reactive oxygen species production in the myometrium

et al. 2015

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Preterm birth is an inflammatory process resulting from the massive infiltration of innate immune cells and the production of proinflammatory cytokines in the myometrium. However, proinflammatory cytokines, which induce labor in vivo, fail to induce labor-associated features in human myometrial cells (MCs). We thus aimed to investigate if reactive oxygen species (ROS) production could be the missing step between immune cell activation and MC response. Indeed, we found that ROS production is increased in the human preterm laboring myometrium (27% ROS producing cells, respectively, versus 2% in nonlaboring controls), with 90% ROS production in macrophages. Using LPS-stimulated myometrial samples and cell coculture experiments, we demonstrated that ROS production is required for labor onset. Furthermore, we showed that ROS are required first in the NADPH oxidase (NADPHox)-2/NF-kB-dependent macrophage response to inflammatory stimuli but, more importantly, to trigger macrophage-induced MCs transactivation. Remarkably, in a murine model of LPS-induced preterm labor (inducing delivery within 17 hours, with no pup survival), cotreatment with glutathione delayed labor onset up to 94 hours and prevented in utero fetal distress, allowing 46% pups to survive. These results suggest that targeting ROS production with the macrophage-permeable antioxidant glutathione could constitute a promising strategy to prevent preterm birth.-Hadi, T., Bardou, M., Mace, G., Sicard, P., Wendremaire, M., Barrichon, M., Richaud, S., Demidov, O., Sagot, P., Garrido, C., Lirussi, F. Glutathione prevents preterm parturition and fetal death by targeting macrophage-induced reactive oxygen species production in the myometrium. FASEB J. 29, 2653-2666 (2015). www.fasebj.org

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NADPH oxidase as an important source of reactive oxygen species at the mouse maternal–fetal interface: putative biological roles

Cited by 25 publications

References 87 publications

Comparative Proteomic Profile of the Human Placenta in Normal and Fetal Growth Restriction Subjects

Comparative Proteomic Profile of the Human Placenta in Normal and Fetal Growth Restriction Subjects

Deficient Vitamin E Uptake During Development Impairs Neural Tube Closure in Mice Lacking Lipoprotein Receptor SR-BI

Glutathione prevents preterm parturition and fetal death by targeting macrophage‐induced reactive oxygen species production in the myometrium

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