Immuno-electron Microscopic Localization of Endothelial Nitric Oxide Synthase in Human Placental Terminal Villous Trophoblasts—Normal and Pre-eclamptic Pregnancy

Matsubara, Shigeki; Tajima, Toshihiro; Takayama, Tadateru; Izumi, Akio; Watanabe, Takushi X.; Sato, Ikuo

doi:10.1053/plac.2001.0718

Cited by 18 publications

(12 citation statements)

References 12 publications

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“…eNOS was detected at the syncytiotrophoblast and endothelium of fetal vessels in control explants without the parasite ( Figure 1A), as already described, 24,44 and T. cruzi did not modify this localization. eNOS was detected at the syncytiotrophoblast and endothelium of fetal vessels in control explants without the parasite ( Figure 1A), as already described, 24,44 and T. cruzi did not modify this localization.…”

Section: The Expression Of Placental Chorionic Villi Nitric Oxide Ssupporting

confidence: 85%

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Nitric oxide synthase and oxidative‐nitrosative stress play a key role in placental infection by Trypanosoma cruzi

Triquell

Díaz-Luján

Romanini

et al. 2018

American J Rep Immunol

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The higher number of parasites caused deleterious consequences to the placental barrier, and the inhibitors (l-NAME and NAC) prevented the damage caused by trypomastigotes in placental villi but not that of the infection. Moreover, trophoblast eNOS played a key role in placental infection with the highest inoculum of Lucky, demonstrating the importance of the enzyme and nitrosative-oxidative stress in Chagas congenital transmission.

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Section: The Expression Of Placental Chorionic Villi Nitric Oxide Ssupporting

confidence: 85%

“…[22][23][24] is an important cellular signaling molecule, 25,26 and it has also been demonstrated that NO is deleterious to the epimastigote and trypomastigote forms of T. cruzi. [22][23][24] is an important cellular signaling molecule, 25,26 and it has also been demonstrated that NO is deleterious to the epimastigote and trypomastigote forms of T. cruzi.…”

mentioning

confidence: 99%

Nitric oxide synthase and oxidative‐nitrosative stress play a key role in placental infection by Trypanosoma cruzi

Triquell

Díaz-Luján

Romanini

et al. 2018

American J Rep Immunol

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“…Furthermore, placental hypoxia, which is associated with pre‐eclampsia, did not induce an upregulation of eNOS to compensate for the reduced blood flow. The present study also demonstrated the presence of eNOS in decidual extravillous trophoblast cells, as well as providing further evidence for the localization of eNOS in villous syncytiotrophoblast cells and the presence of eNOS mRNA expression and transcription in the human placenta 6,7,20–22 . A limitation of the present study was the unmatched gestational age between the NP and pre‐eclamptic group.…”

Section: Discussionmentioning

confidence: 50%

Placental endothelial nitric oxide synthase localization and expression in normal human pregnancy and pre‐eclampsia

Orange¹,

D²,

Horvath³

et al. 2003

Clin Exp Pharma Physio

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1. The aim of the present study was to investigate whether pre-eclampisa, a state of placental hypoxia, is associated with placental abnormalities in the amount, distribution and expression of endothelial nitric oxide synthase (eNOS). 2. Localization and intensity of eNOS was determined by immunohistochemistry using an antibody specific for eNOS. The amount of eNOS mRNA expression was determined by reverse transcription-polymerase chain reaction (RT-PCR) and the densitometry of gel bands was expressed as a ratio of the band density of the housekeeping gene beta2-microglobulin. 3. Endothelial NOS staining was localized to syncytiotrophoblast cells within the villi and decidual trophoblast cells. It was not present in the endothelium of terminal villous vessels. There was no significant difference in eNOS villous or decidual staining intensity between normal pregnancy (NP; n = 12), pre-eclampsia (n = 14), or gestational hypertension (GH; n = 4). Staining for eNOS was not significantly different in the decidua compared with the villi in NP, GH or pre-eclampsia. Within the decidua, the depth of eNOS staining was similar in NP, pre-eclampisa and GH. 4. There was no significant difference in eNOS mRNA expression between NP (0.70 +/- 0.11), pre-eclampsia (0.5 +/- 0.07) or GH (0.69 +/- 0.26). 5. These findings suggest that the amount of eNOS in the placenta is not deficient in pre-eclampsia, excluding a possible pathogenic role for eNOS in this disease. Furthermore, placental hypoxia, which is associated with pre-eclampsia, did not induce an upregulation of eNOS

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“…Of those, 15 were excluded, 7 did not include sufficient data (Matsubara et al, 2001;Savvidou et al, 2001;Hingorani, 2003;Yu et al, 2003;Donker et al, 2005;Corthorn et al, 2006;Barut et al, 2010;Best et al, 2010), 4 were not published in English (Tong et al, 1998;Zhou et al, 1998Zhou et al, , 2003Kukor and Valent, 2010), 2 were letters (Moreno, 2008;Seremak-Mrozikiewicz et al, 2008), 1 did not include control group (Hocher et al, 2008), 1 was a review (Hingorani, 2003), and 25 were considered eligible for the metaanalysis. Of those, seven studies were excluded (Kobashi et al, 2001;Grandone et al, 2003;Tempfer et al, 2004;Chen et al, 2007;Nishizawa et al, 2009;Singh et al, 2010;Sharma et al, 2011), because the distribution of the genotypes in the control group was not in HWE ( p < 0.05).…”

Section: Study Selectionmentioning

confidence: 99%

Endothelial Nitric Oxide Synthase Gene Polymorphisms (G894T, 4b/a and T-786C) and Preeclampsia: Meta-Analysis of 18 Case–Control Studies

Chen

Zhao

Sun

et al. 2012

DNA and Cell Biology

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Studies investigating the association between endothelial nitric oxide synthase (eNOS) gene polymorphisms and preeclampsia reported contradictory or nonconclusive results. We performed a meta-analysis of 18 genetic association studies that examined the relationship between preeclampsia and the G894T, 4a/b and T-786C polymorphisms of the eNOS gene. Subgroup analysis by ethnicity and potential sources of heterogeneity and bias were explored. The MEDLINE, EMBASE, and Google Scholar databases were searched to access the relevant genetic association studies up to June 2011. For the allelic analysis of the G894T variant, all studies showed no significant association. For the genotypic analysis, the combined studies of the G allele showed negative significance (odds ratio [OR]=0.56; 95% confidence interval [CI]: 0.33-0.97), all the studies showed positively significance when the T allele was combined (OR=1.17; 95% CI: 1.01-1.36), and results were also positively significant in non-Asian populations (OR=1.20; 95% CI: 1.02-1.43). For the allelic analysis of the 4b/a variant, all studies showed no significant association, but results were negatively significant in non-Asian populations (OR=0.67; 95% CI: 0.46-0.98). For the genotype analysis, combined studies of the b allele showed negative significance (OR=0.55; 95% CI: 0.36-0.84). Moreover, non-Asian studies showed negatively significant results (OR=0.45; 95% CI: 0.28-0.72). For the analysis of the T-786C variant, none of the studies showed significant results. The synthesis of available evidence supports the fact that intron 4a allele, homozygosity for the 894T and intron 4a of eNOS are positively associated with preeclampsia. Large, multiethnic confirmatory, and well-designed studies are needed to determine the relation between preeclampsia and polymorphisms of the eNOS gene.

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Immuno-electron Microscopic Localization of Endothelial Nitric Oxide Synthase in Human Placental Terminal Villous Trophoblasts—Normal and Pre-eclamptic Pregnancy

Cited by 18 publications

References 12 publications

Nitric oxide synthase and oxidative‐nitrosative stress play a key role in placental infection by Trypanosoma cruzi

Nitric oxide synthase and oxidative‐nitrosative stress play a key role in placental infection by Trypanosoma cruzi

Placental endothelial nitric oxide synthase localization and expression in normal human pregnancy and pre‐eclampsia

Endothelial Nitric Oxide Synthase Gene Polymorphisms (G894T, 4b/a and T-786C) and Preeclampsia: Meta-Analysis of 18 Case–Control Studies

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