Expression of nitric oxide synthase by syncytiotrophoblast in human placental villi

Conrad, Kirk P.; Vill, Maggie; McGuire, Paul; Dail, William G.; Davis, Alan K.

doi:10.1096/fasebj.7.13.7691671

Cited by 142 publications

(104 citation statements)

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“…In addition, the data show that NO production reached a peak at day 15.5 of gestation and declined during the last few days of gestation, as NO production in the 15.5-day placenta was 2.6-fold greater than that of the term placenta. Although several studies have demonstrated the presence of NOS in the placenta [5,13,14,23], to the best of our knowledge, the present study is the first report that shows the developmental time-course of NO production in the rat placenta during pregnancy.…”

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confidence: 57%

Gestational Changes in Production of NO and Expression of NOS mRNA Isoforms in the Rat Placenta

et al. 2009

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ABSTRACT. To monitor changes in NO production over time in the fetal placenta of rats, we used electron paramagnetic resonance spectroscopy with the Fe-N-(dithiocarboxy) sarcosine (Fe-DTCS) complex as an NO-trapping reagent. The expression of nitric oxide synthase (NOS) isoforms was examined in parallel using quantitative RT-PCR. NO production was first detected on day 13.5 of gestation. NO levels reached a peak on day 15.5, then decreased significantly during the last few days of gestation. The pattern of expression of NOS II mRNA was in good agreement with changes in NO levels, whereas NOS III mRNA expression did not change markedly during gestation. Thus, it appears that NO levels in the placenta are NOS II-dependent and differ at different gestational stages. KEY WORDS: electron paramagnetic resonance (EPR), fetal placenta, nitric oxide.

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confidence: 57%

Gestational Changes in Production of NO and Expression of NOS mRNA Isoforms in the Rat Placenta

et al. 2009

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“…Indeed, it was recently shown that the eNOS promoter contains a hypoxia response element and thus might be a HIF target gene (11). Expression of iNOS and eNOS has been observed in human and murine placenta (10,41,45). Thus hypoxic upregulation of placental NOS expression may result in NO-mediated vasodilation, thereby increasing placental blood flow and reconstituting oxygen supply to the placenta.…”

Section: Discussionmentioning

confidence: 99%

Preserved placental oxygenation and development during severe systemic hypoxia

Schäffer¹,

Vogel²,

Breymann³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The placenta is capable of generating NOs, 17 which can in turn react with superoxide to form peroxynitrite anions (ONOO Ϫ ) that covalently modify proteins by nitration of tyrosine residues. 18 Accordingly, we also used immunolocalization techniques to determine whether the apparent preeclampsia-associated changes in invasive cytotrophoblast XDH/XO staining and XO activity were accompanied by changes in the oxidative status of the tissue.…”

Section: The Effects Of Preeclampsia On Nitrotyrosine Generation By Cmentioning

confidence: 99%

Invasive Cytotrophoblasts Manifest Evidence of Oxidative Stress in Preeclampsia

Many

Hubel

Fisher

et al. 2000

The American Journal of Pathology

255

150

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In preeclampsia, poor placental perfusion may result in maternal endothelial dysfunction, but the pathways involved are largely unknown. Candidate placental mediators include products of oxidative stress released into the maternal circulation. Xanthine oxidase has been implicated in postischemic-reperfusion injury via the generation of superoxide anion radicals (superoxide; O 2 .؊ ) and hydrogen peroxide. We examined placentas and placental bed curettings and/or biopsies from preeclamptic control pregnant women to test the hypothesis that xanthine oxidase is a mediator of oxidative stress in placentas from women with preeclampsia. The expression of xanthine dehydrogenase/xanthine oxidase holoenzyme and the activity of xanthine oxidase, the isoform known to generate reactive oxygen species, were increased in a subpopulation of cytotrophoblasts of preeclamptic women. Additionally, the expression of superoxide dismutase, which would scavenge superoxide produced by xanthine oxidase, was reduced in the same cells. Preeclampsia, a pregnancy-specific disorder, is the leading cause of maternal mortality in the Western world and increases perinatal mortality fivefold. The clinical diagnosis is based on the new onset of hypertension and the appearance of proteinuria and edema during pregnancy. It is evident, however, that these findings are a small component of a multisystemic disease that reduces perfusion to virtually all of the organs in the body. 1 The hypothesis has been advanced that much of the disease could be explained by alterations in the function of vascular endothelium. Increasing data support this hypothesis. 2 The more complete hypothesis posits that the placenta, likely in response to reduced perfusion, produces a circulating factor(s) that alters endothelial cell function. 2 Among the candidate molecules are products resulting from oxidative stress. 3 Oxidative stress, the result of freeradical generation in excess of protective mechanisms, is suggested as an important component of other disorders that affect endothelial function, including diabetes and atherosclerosis. 4,5 Evidence for oxidative stress in preeclampsia includes elevated lipid hydroperoxides or their metabolites and reduced plasma antioxidant activity. 3,6 -8 Xanthine oxidase, which metabolizes xanthine and hypoxanthine to uric acid with production of superoxide and hydrogen peroxide, is an integral mediator of reactive oxygen species generation in many settings. Usually, this enzyme is present as the holoenzyme xanthine dehydrogenase/xanthine oxidase (XDH/XO). The dehydrogenase isoform (XDH) converts purines to uric acid with reducton of nicotinamide-adenine dinucleotide (NAD) to reduced NAD (NADH). With hypoxia and in response to several cytokines, XDH/XO synthesis increases, and the conversion of the enzyme to the XO form is enhanced. 9 Reduced organ perfusion and subsequent reperfusion are proposed to result in increased XO during reduced flow and in subsequent formation of reactive oxygen species with reperfusion. The inadequate pla...

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Expression of nitric oxide synthase by syncytiotrophoblast in human placental villi

Cited by 142 publications

References 0 publications

Gestational Changes in Production of NO and Expression of NOS mRNA Isoforms in the Rat Placenta

Gestational Changes in Production of NO and Expression of NOS mRNA Isoforms in the Rat Placenta

Preserved placental oxygenation and development during severe systemic hypoxia

Invasive Cytotrophoblasts Manifest Evidence of Oxidative Stress in Preeclampsia

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