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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of exposure to various oxygen tensions on villi in organ culture are re-examined. Villi from ten normal mature placentae were cultured under hypoxic (6 per cent oxygen) and hyperoxic (40 per cent oxygen) conditions for 6 or 12 h. Control tissue (zero time in culture) was also taken. Pieces of tissue were fixed by immersion and embedded in resin for semithin sectioning. Systematically sampled microscopical fields were analysed stereologically to estimate harmonic and arithmetic mean thicknesses for the trophoblast and for the villous membrane and to assess the volumetric composition and mean diameter of villi. Trophoblast thicknesses were influenced significantly by oxygen tension, being smaller in hypoxic and greater in hyperoxic media. No significant interaction terms or effects of time in culture were detected. Villous membrane thicknesses altered in a similar fashion to trophoblast thicknesses. No significant differences in the composition of villi were detected but villi tended to be greater in diameter during hyperoxia. Findings are discussed in the context of previously reported adaptations in vivo, in different regions of the placental lobule and during chronic maternal hypoxic stress at high altitude. We conclude that there is insufficient evidence to support the claim that villi can adapt in vitro to varying ambient oxygen tensions.
Placenta
PMID:Stereological re-examination of the effects of varying oxygen tensions on human placental villi maintained in organ culture for up to 12 h. 277 96

Morphological studies show poor placental vascular development and an increase in the mitotic index of cytotrophoblast cells in intrauterine growth restriction (IUGR). We hypothesized that the reported relatively high oxygen level in the intervillous space in contact with IUGR placental villi will limit angiogenesis by changes in vascular endothelial growth factor (VEGF) and placenta growth factor (PIGF) expression and function. Western immunoblot analysis demonstrates a diametric expression of PIGF and VEGF proteins throughout pregnancy, with P1GF levels increasing and VEGF levels decreasing, consistent with placental oxygenation. PIGF mRNA and protein is increased in IUGR as compared to gestationally matched normal placentae. Increasing oxygen tension upregulates P1GF protein in term placental villous explants, whereas hypoxia downregulates P1GF and VEGFR-1 (Flt-1) autophosphorylation in term trophoblast choriocarcinoma cell line (BeWo). Levels of soluble Flt-1 (sFlt-1) protein in supernatant of term villous explants were upregulated by 1 per cent hypoxia, whereas hyperoxia (40 per cent) decreased sFlt-1 levels, indicating that under conditions of increasing oxygen tension, PlGF function may remain unopposed. The addition of PlGF-1 to a spontaneously transformed first trimester cytotrophoblast cell line (ED27) stimulated cell proliferation while PlGF-2 had little effect. In contrast, the addition of PlGF-1 had little effect on endothelial cell proliferation while this was inhibited by PIGF-2. Taken together these changes provide a molecular explanation for the observed poor angiogenesis in the pathogenesis of IUGR.
Placenta
PMID:Regulation of placental vascular endothelial growth factor (VEGF) and placenta growth factor (PIGF) and soluble Flt-1 by oxygen--a review. 1083 Nov 17

At term of pregnancy, oxygen consumption by the human or ovine placenta accounts for 40 per cent of total oxygen uptake by the gravid uterus. In the sheep, most oxygen is used for oxidative phosphorylation of glucose; the remainder is probably utilized for non-mitochondrial processes. The ATP yield is expended mainly in protein synthesis and cation transport. The fractional protein synthesis rate of ovine placenta is 60 per cent per day. Applying these data to man, protein synthesis is estimated to account for about 30 per cent of placental oxygen uptake. Probably this reflects the high rates of synthesis of peptide and steroid hormones. The Na+ gradient is the basis for secondary active transport of amino acids and other substances, and the Na(+)-K(+)-pump probably accounts for 20-30 per cent of oxygen uptake, with a smaller contribution from Ca(2+)-ATPase. Placental oxygen uptake remains constant during acute reductions in uterine oxygen supply and is maintained at the expense of the fetus. In the longer term, in experimental models of fetal growth restriction, placental oxygen consumption is reduced to a greater extent than fetal oxygen consumption. Placental oxygen consumption is greatly reduced under in vitro experimental conditions, due largely to an inadequate oxygen supply. This results in reduced protein synthesis and possibly inhibition of Na(+)-K(+)-ATPase. However, if the placenta is subjected to hyperoxia, by raising the PO2 of the medium, there is an increase in anaerobic glycolysis and structural damage may ensue. Premature exposure of trophoblast to high oxygen tensions in vivo may result in reduced villous branching, but this is likely to be a cause, rather than a consequence, of reduced fetal growth and oxygen consumption.
Placenta
PMID:Placental oxygen consumption. Part I: in vivo studies--a review. 1083 Nov 19

The syncytiotrophoblast contains aggregates of nuclei termed syncytial knots. Increased numbers of syncytial knots have been reported in placentae of pregnancies complicated by pre-eclampsia and fetal growth restriction (FGR). As oxidative stress has been implicated in the pathophysiology of these disorders, we hypothesised that the formation of syncytial knots may be induced by exposure to hypoxia, hyperoxia or reactive oxygen species (ROS). We assessed both the number and morphology of syncytial knots induced by culture in hypoxia, hyperoxia and with ROS. We also investigated whether the presence of syncytial knots in normal tissue was associated with a down-regulation of anti-apoptotic proteins Bcl-2, Mdm2, XIAP and survivin. Using our measurement system we describe an increased number of syncytial knots when tissue is cultured in hypoxia, hyperoxia or in the presence of ROS. The morphology of these syncytial knots was similar to those seen in vitro, although the nuclei from cultured placental explants were morphologically more homogenous, had fewer nuclear pores, and a higher heterochromatin:euchromatin ratio. Despite the apoptotic appearances of nuclei we did not detect a loss of anti-apoptotic proteins in the region of syncytial knots. We conclude that the increased number of syncytial knots in placentae from pregnancies complicated by pre-eclampsia and FGR can be replicated in vitro by ROS or hypoxia, supporting their involvement in the pathogenesis of these conditions.
Placenta 2007 Apr
PMID:Formation of syncytial knots is increased by hyperoxia, hypoxia and reactive oxygen species. 1714 Jun 57

Gene expression studies have demonstrated the altered expression level of placental angiogenesis related genes in severe pre-eclampsia (PE). In cord compression, the transportation of oxygen from the placenta to the fetus is blocked, and it is speculated that during blockade the originally hypoxic placenta may become hyperoxic. We compared the placental gene expression profiles of one pre-eclamptic patient with cord compression (the index patient) to the profiles of patients with PE and those of normal pregnancy controls (including one woman with cord compression). The gene expression of the cord compression PE patient resembled that observed in the normal pregnancies. We hypothesize that umbilical blockade may in a short period of time lead to placental hyperoxia, which in turn has an effect on angiogenic gene expression profile.
Placenta 2008 May
PMID:Cord compression may rapidly influence the expression of placental angiogenic genes in pre-eclampsia. 1838 71

Oxygen (O(2)) is essential for aerobic life; however, the level of O(2), whether too low (hypoxia) or too high (hyperoxia), can induce oxidative injury and increase morbidity and mortality. Disruption of O(2) homeostasis represents a major aspect of many disease etiologies and pathobiology. In the past, our laboratory has been using Drosophila melanogaster to investigate the cellular and molecular aspects of the response to hypoxia and oxidative stress. There are several advantages for using Drosophila as a model system, the most important one being an evolutionary conservation of genetic and signaling pathways from Drosophila to mammals. As a proof of this concept, we have shown that we can substantially improve the tolerance of human cells in culture by transfecting these cells with particular Drosophila genes. In this review, we summarize the recent findings from our laboratory using Drosophila as a model system to investigate the genetic basis of hypoxia/hyperoxia tolerance. We have done microarray studies and identified several oxidative stress resistance genes that play an important role in individual paradigms such as constant or intermittent hypoxia, short term (days) or long term (generations) hypoxia/hyperoxia. Our studies provide evidence that a pattern of oxidative stress is specific in inducing a gene expression profile which, in turn, plays an important role in modulating the phenotype. To improve our understanding of oxidative and hypoxic stress as well as its associated diseases, multi-disciplinary approaches are necessary and critical in the study of complicated issues in systems biology.
Placenta 2011 Mar
PMID:Review: Hypoxic and oxidative stress resistance in Drosophila melanogaster. 2135 99

The Human Placenta Project has focused attention on the need for noninvasive magnetic resonance imaging (MRI)-based techniques to diagnose and monitor placental function throughout pregnancy. The hope is that the management of placenta-related pathologies would be improved if physicians had more direct, real-time measures of placental health to guide clinical decision making. As oxygen alters signal intensity on MRI and oxygen transport is a key function of the placenta, many of the MRI methods under development are focused on quantifying oxygen transport or oxygen content of the placenta. For example, measurements from blood oxygen level-dependent imaging of the placenta during maternal hyperoxia correspond to outcomes in twin pregnancies, suggesting that some aspects of placental oxygen transport can be monitored by MRI. Additional methods are being developed to accurately quantify baseline placental oxygenation by MRI relaxometry. However, direct validation of placental MRI methods is challenging and therefore animal studies and ex vivo studies of human placentas are needed. Here we provide an overview of the current state of the art of oxygen transport and quantification with MRI. We suggest that as these techniques are being developed, increased focus be placed on ensuring they are robust and reliable across individuals and standardized to enable predictive diagnostic models to be generated from the data. The field is still several years away from establishing the clinical benefit of monitoring placental function in real time with MRI, but the promise of individual personalized diagnosis and monitoring of placental disease in real time continues to motivate this effort.
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PMID:Placental MRI: Developing Accurate Quantitative Measures of Oxygenation. 3159 95