Expression of NADPH Oxidase by Trophoblast Cells: Potential Implications for the Postimplanting Mouse Embryo1

Gomes, Sara Zago; Lorenzon-Ojea, Aline R.; Vieira, Juliana Siviero; Rocha, Clarissa Ribeiro Reily; Bandeira, Carla Letícia; Hoshida, Mara Sandra; Lopes, Lucia Rossetti; Bevilacqua, Estela

doi:10.1095/biolreprod.111.094748

Cited by 11 publications

(13 citation statements)

References 46 publications

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“…The H2O2 production from the surface of trophectodermal cells is proposed to participate in the interaction of hatched blastocyst and the endometrium in the decidual response (Manes and Lai, 1995) due to Nox activity. All the components required for the Nox complex are expressed in the trophectodermal cells (Gomes et al, 2012) supporting the proposal that ROS also participate in the implantation of the blastocyst (Bevilacqua et al, 2012).…”

Section: Oxygen and Ros In Animal Developmentsupporting

confidence: 75%

Oxygen, reactive oxygen species and developmental redox networks: Evo-Devo Evil-Devils?

Salas‐Vidal¹,

Méndez-Cruz²,

Ramírez-Corona³

et al. 2021

Int. J. Dev. Biol.

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Molecular oxygen (O2), reactive oxygen species (ROS), and associated redox networks are cornerstones of aerobic life, these molecules and networks have gained recognition as fundamental players in mechanisms that regulate the development of multicellular organisms. First, we present a brief review in which we provide a historical description of some relevant discoveries that led to this recognition. We also discuss that despite its abundance in nature, oxygen is a limiting factor, and its high availability variation impacted the evolution of adaptive mechanisms to guarantee the proper development of diverse species under such extreme environments. Finally, some examples when oxygen and ROS were identified as relevant for the control of developmental processes are discussed. We take into account not only the current knowledge on animal redox developmental biology, but also briefly discuss potential scenarios on the origin and evolution of redox developmental mechanisms and the importance of the ever-changing environment.

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Section: Oxygen and Ros In Animal Developmentsupporting

confidence: 75%

Oxygen, reactive oxygen species and developmental redox networks: Evo-Devo Evil-Devils?

Salas‐Vidal¹,

Méndez-Cruz²,

Ramírez-Corona³

et al. 2021

Int. J. Dev. Biol.

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“…Still in mice, but in later gestational stages, neither NADPH oxidase nor XO inhibitors are able to completely abolish ROS production in ectoplacental cone cells: these findings indicate that both ROS production systems are active in trophoblast cells (Gomes et al, 2011). In addition, studies focusing on antioxidant defences in the rat placenta showed increased placental activity of XO between gd16 and 22, suggesting that placental XO-mediated ROS generation increases in late gestation (Jones et al, 2010).…”

Section: Xanthine Oxidasementioning

confidence: 90%

“…The molecular characterization of the mouse trophoblast NADPH oxidase that gives greater insight into the functional enzymic activity in placental tissues comes from Gomes et al (2011). They have shown that ectoplacental cone cells express the essential elements for the activation of NADPH oxidase: the membrane subunits, gp91phox and p22phox that contain the catalytic domain in the enzyme; the cytosolic subunits p40phox that can function as a regulatory factor; p47phox whose phosphorylation is essential for the enzyme activation; p67phox (an obligatory component); and the G-protein Rac1, reinforcing the potential enzymic activity of the trophoblast.…”

Section: Nadph Oxidase and Ros Generation At The Maternal-fetal Interfacementioning

confidence: 99%

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

Bevilacqua

Gomes

Lorenzon-Ojea

et al. 2012

Reproductive BioMedicine Online

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Oxygen derivatives that comprise the large family of reactive oxygen species (ROS) are actively involved in placental biology. They are generated at the maternal-fetal interface at the level of decidual, trophoblast and mesenchymal components. In normal conditions, ROS produced in low concentrations participate in different functions as signalling molecules, regulating activation of redox-sensitive transcription factors and protein kinases involved in cell survival, proliferation and apoptosis, hence much of cell functioning. Physiological ROS generation is also associated with such defence mechanisms as phagocytosis and microbiocidal activities. In mice, particularly but not exclusively, trophoblast cells phagocytose intensively during implantation and post-implantation periods and express enzymic machinery to address a ROS-producing response to changes in the environment. The cells directly associated with ROS production are trophoblast giant cells, which mediate each and every relationship with the maternal organism. In this review, the production of ROS by the implanting mouse trophoblast is discussed, focusing on NADPH oxidase expression, regulatory mechanisms and similarities with NOX2 from phagocytes. Some of the current controversies are assessed by attempting to integrate data from studies in human trophoblast and mouse models.

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“…The inhibitory action of apocynin on the effects on HG indicates an important role of NOX in mediating the effects of HG. Functional NOX has been observed in mouse ectoplacental cones of 7.5 GD conceptuses and in cultured TGCs derived from these cones (Bevilacqua, Hoshida, Amarante‐Paffaro, Albieri‐Borges, & Gomes, , Gomes et al, ). ROS generation by NOX has been associated with the phagocytic activity of the post‐implantation trophoblast (Gomes et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…Functional NOX has been observed in mouse ectoplacental cones of 7.5 GD conceptuses and in cultured TGCs derived from these cones (Bevilacqua, Hoshida, Amarante‐Paffaro, Albieri‐Borges, & Gomes, , Gomes et al, ). ROS generation by NOX has been associated with the phagocytic activity of the post‐implantation trophoblast (Gomes et al, ). In this study, apocynin prevented the HG‐induced increases in PLAU, PAI‐1, and MMP‐9 expression, decreasing trophoblast spreading.…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia‐induced mouse trophoblast spreading is mediated by reactive oxygen species

Sánchez-Santos

Martínez-Hernández

Contreras-Ramos³

et al. 2018

Molecular Reproduction Devel

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During embryo implantation, the outer layer of the blastocyst interacts with the endometrium giving rise to the development of the trophoblast cell lineage. The cells in this lineage participate in the penetration of endometrium due to their motility and invasive properties. The mechanisms that regulate the differentiation and invasive ability of these cells are essential for the establishment and maintenance of an efficient exchange between maternal and fetal tissues during pregnancy. In this context, hyperglycemia can induce oxidative stress causing alterations in the placenta. This study evaluated the role of reactive oxygen species (ROS) in the actions of high glucose concentration (HG) on trophoblast spreading and the expression of extracellular proteases in cultured mouse conceptuses. Blastocysts from gestational day 4 (GD4) were cultured until GD7 in HAM-F10 medium and further treated for 48 hr with HG (25 mM glucose) from GD7 to GD9. This treatment induced larger trophoblast outgrowths and increased ROS concentration, which was associated with increased expression levels of urokinase-type plasminogen activator (PLAU), plasminogen activator inhibitor 1 (PAI-1), and matrix metalloproteinase 9 (MMP-9). These effects were prevented by treatment with the non-specific antioxidant N-acetylcysteine (NAC) or apocynin, an inhibitor of NADPH oxidase. Our data suggest that the HG-induced trophoblast spreading and the expression of PLAU, PAI-1, and MMP-9 were mediated by the production of ROS via NADPH oxidase activity. Our results shed light on placental alterations in gestational diabetes mellitus.

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Expression of NADPH Oxidase by Trophoblast Cells: Potential Implications for the Postimplanting Mouse Embryo1

Cited by 11 publications

References 46 publications

Oxygen, reactive oxygen species and developmental redox networks: Evo-Devo Evil-Devils?

Oxygen, reactive oxygen species and developmental redox networks: Evo-Devo Evil-Devils?

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

Hyperglycemia‐induced mouse trophoblast spreading is mediated by reactive oxygen species

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