Fetal Growth Retardation
|
0.690 |
Biomarker
|
phenotype |
BEFREE |
We tested the hypothesis that melatonin would increase fetal growth in two mouse models of FGR which together represent a spectrum of the placental phenotypes in this complication: namely the endothelial nitric oxide synthase knockout mouse (eNOS<sup>-/-</sup>) which presents with abnormal uteroplacental blood flow, and the placental specific <i>Igf2</i> knockout mouse (P0<sup>+/-</sup>) which demonstrates aberrant placental morphology akin to human FGR.
|
30158878 |
2018 |
Fetal Growth Retardation
|
0.690 |
Biomarker
|
phenotype |
CTD_human |
We hypothesized that treatment of endothelial nitric oxide synthase knockout mice (eNOS⁻/⁻) and catechol-O-methyltransferase knockout mice (COMT⁻/⁻) with resveratrol during pregnancy would improve uterine artery blood flow and therefore ameliorate the PE-like phenotype and FGR in these murine models.
|
23667712 |
2013 |
Fetal Growth Retardation
|
0.690 |
GeneticVariation
|
phenotype |
BEFREE |
We analyzed the Glu298Asp polymorphism of the endothelial nitric oxide synthase gene and asymmetric dimethylarginine (ADMA) in 55 Turkish patients with PE without fetal growth retardation (FGR) and in 54 healthy pregnant women.
|
20598027 |
2010 |
Fetal Growth Retardation
|
0.690 |
Biomarker
|
phenotype |
BEFREE |
We aimed to determine the effects of maternal antioxidant treatment with N-acetylcysteine (NAC) on fetal endothelial function and endothelial nitric oxide synthase (eNOS) programming in IUGR guinea pigs.
|
27739590 |
2017 |
Fetal Growth Retardation
|
0.690 |
Biomarker
|
phenotype |
BEFREE |
The nitric oxide donor 2-[[4-[(nitrooxy)methyl]benzoyl]thio]-benzoic acid methyl ester (SE175) induced significant relaxation of mouse uterine arteries and human placental arteries <i>in vitro</i>; thus, SE175 was encapsulated into these targeted liposomes and administered to healthy pregnant C57BL/6J mice or endothelial nitric oxide synthase knockout (eNOS<sup>-/-</sup>) mice, which exhibit impaired uteroplacental blood flow and FGR.
|
29109771 |
2017 |
Fetal Growth Retardation
|
0.690 |
AlteredExpression
|
phenotype |
BEFREE |
Our results indicated that IUGR reduced vasodilation via acetylcholine in aorta rings, decreased NO levels, and increased eNOS phosphorylation at Thr495.
|
28689502 |
2017 |
Fetal Growth Retardation
|
0.690 |
AlteredExpression
|
phenotype |
BEFREE |
Normal or IUGR HUVEC monolayers were exposed (0-24h) to 5% O(2) (normoxia), and 1 or 2% O(2) (hypoxia). l-Arginine transport and hCAT-1 expression, phosphorylated and total PKCalpha or eNOS protein and mRNA expression were quantified. eNOS involvement was tested using a siRNA against eNOS (eNOS-siRNA) adenovirus.
|
19501907 |
2009 |
Fetal Growth Retardation
|
0.690 |
Biomarker
|
phenotype |
RGD |
Intrauterine growth restriction and shallower implantation site in rats with maternal hyperinsulinemia are associated with altered NOS expression.
|
19709742 |
2009 |
Fetal Growth Retardation
|
0.690 |
AlteredExpression
|
phenotype |
BEFREE |
Elevated expression of ecNOS was found to be coupled with significantly lower SOD activity and glutathione level, and increased lipid peroxidation in IUGR neonates.
|
19779107 |
2009 |
Fetal Growth Retardation
|
0.690 |
Biomarker
|
phenotype |
BEFREE |
Compared with HUVECs from normal newborns, nitric oxide (NO) production was reduced, with imbalance between endothelial nitric oxide synthase (eNOS) and arginase-2 (Arg-2) in IUGR.
|
30392707 |
2018 |
Fetal Growth Retardation
|
0.690 |
Biomarker
|
phenotype |
RGD |
Arginase upregulation and eNOS uncoupling contribute to impaired endothelium-dependent vasodilation in a rat model of intrauterine growth restriction.
|
29741931 |
2018 |
Fetal Growth Retardation
|
0.690 |
GeneticVariation
|
phenotype |
BEFREE |
Altogether, these data suggest that adult vascular dysfunction in the FGR does not result from early changes in Nos3 promoter DNA methylation, but from an altered vessel structure established during foetal development.
|
31177629 |
2019 |
Fetal Growth Retardation
|
0.690 |
Biomarker
|
phenotype |
HPO |
|
|
|