Expression of NO synthases and redox enzymes in umbilical arteries from newborns born small, appropriate, and large for gestational age

Abstract

Background: Modified expression of nitric oxide synthases (NOss) and an imbalance between the pro-oxidative and the antioxidative system accompany endothelial dysfunction, the first stage of atherosclerosis. humans born small (sGa) or large (LGa) for gestational age are at higher risk of developing atherosclerosis later in life than humans born appropriate for gestational age (aGa). We hypothesized that indicators of endothelial dysfunction could be detectable at birth. The purpose of this study was to find out whether the expression patterns of NO synthases (endothelial NOs (eNOs), inducible NOs (iNOs), and neuronal NOs (nNOs)), pro-oxidative enzymes (components of nicotinamide adenine dinucleotide phosphate (NaDPh) oxidases, NaDPh oxidase 1 (NOX1), NOX2, NOX4, p22phox, and p47phox), and antioxidative enzymes (superoxide dismutase 1-3 (sOD1-3), glutathione peroxidase 1 (GPX1), and catalase) in umbilical arteries differ among sGa, LGa, and aGa newborns. Methods: Thirty-six umbilical cords were obtained from healthy, normal, full-term sGa, aGa, and LGa newborns. The umbilical arteries were dissected and homogenized. mRNa expression was analyzed with quantitative real-time PcR. Western blotting was performed to determine protein expression. results: mRNa and protein expression of NO synthases, prooxidative enzymes, and antioxidative enzymes did not differ in the umbilical arteries from newborns of the three groups. conclusion: Indicators of endothelial dysfunction in terms of differences in enzyme expression in sGa or LGa newborns vs. aGa newborns were not present at birth.

Endothelial dysfunction in individuals born after fetal growth restriction: cardiovascular and renal consequences and preventive approaches

“…31,81 However, these results are controversial because they could not be replicated. 82 Moreover, differences in eNOS expression have been observed in human endothelial cells isolated from the umbilical arteries (HUAECs) or veins (HUVECs) of IUGR newborns. eNOS expression is increased in IUGR-HUAECs but decreased in IUGR-HUVECs.…”

“…In humans, independent studies have indicated that eNOS expression is increased in the umbilical arteries of babies born after fetal growth restriction, suggesting that activated NO synthesis may be a compensatory mechanism to improve placental blood flow 31 81 However, these results are controversial because they could not be replicated 82 . Moreover, differences in eNOS expression have been observed in human endothelial cells isolated from the umbilical arteries (HUAECs) or veins (HUVECs) of IUGR newborns.…”

LGA‐newborn from patients with pregestational obesity present reduced adiponectin‐mediated vascular relaxation and endothelial dysfunction in fetoplacental arteries

“…In this context, we found that eNOS expression is increased in endothelial cells of LGA of obese woman, suggesting a compensatory mechanism to maintain normal NO; however, eNOS activity is not different to control. There are few studies looking at eNOS expression in fetal endothelium of LGA, Dellee, Tobias, Li, and Mildenberger () found no differences in eNOS between LGA and AGA; however, they did not consider maternal BMI. This indicates that MO could increase eNOS protein expression in LGA newborns.…”