Compensatory feto-placental upregulation of the nitric oxide system during fetal growth restriction.
<h4>Background</h4>Fetal Growth Restriction is often associated with a feto-placental vascular dysfunction conceivably involving endothelial cells. Our study aimed to verify this pathogenic role for feto-placental endothelial cells and, coincidentally, demonstrate any abnormality in the...
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doaj-d59bbcc8bcc74fe3a09003051b2691e22021-03-04T00:15:23ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-0179e4529410.1371/journal.pone.0045294Compensatory feto-placental upregulation of the nitric oxide system during fetal growth restriction.Silvia PisaneschiFrancesca A L StriginiAngel M SanchezSilvia BegliuominiElena CasarosaAndrea RipoliPaolo GhirriAntonio BoldriniBruno FinkAndrea R GenazzaniFlavio CoceaniTommaso Simoncini<h4>Background</h4>Fetal Growth Restriction is often associated with a feto-placental vascular dysfunction conceivably involving endothelial cells. Our study aimed to verify this pathogenic role for feto-placental endothelial cells and, coincidentally, demonstrate any abnormality in the nitric oxide system.<h4>Methods</h4>Prenatal assessment of feto-placental vascular function was combined with measurement of nitric oxide (in the form of S-nitrosohemoglobin) and its nitrite byproduct, and of the endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine. Umbilical vein endothelial cells were also harvested to determine their gene profile. The study comprised term pregnancies with normal (n = 40) or small-for-gestational-age (n = 20) newborns, small-for-gestational-age preterm pregnancies (n = 15), and bi-chorial, bi-amniotic twin pregnancies with discordant fetal growth (n = 12).<h4>Results</h4>Umbilical blood nitrite (p<0.001) and S-nitrosohemoglobin (p = 0.02) rose with fetal growth restriction while asymmetric dimethylarginine decreased (p = 0.003). Nitrite rise coincided with an abnormal Doppler profile from umbilical arteries. Fetal growth restriction umbilical vein endothelial cells produced more nitrite and also exhibited reciprocal changes in vasodilator (upwards) and vasoconstrictor (downwards) transcripts. Elevation in blood nitrite and S-nitrosohemoglobin persisted postnatally in the fetal growth restriction offspring.<h4>Conclusion</h4>Fetal growth restriction is typified by increased nitric oxide production during pregnancy and after birth. This response is viewed as an adaptative event to sustain placental blood flow. However, its occurrence may modify the endothelial phenotype and may ultimately represent an element of risk for cardiovascular disease in adult life.https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23028913/pdf/?tool=EBI |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Silvia Pisaneschi Francesca A L Strigini Angel M Sanchez Silvia Begliuomini Elena Casarosa Andrea Ripoli Paolo Ghirri Antonio Boldrini Bruno Fink Andrea R Genazzani Flavio Coceani Tommaso Simoncini |
spellingShingle |
Silvia Pisaneschi Francesca A L Strigini Angel M Sanchez Silvia Begliuomini Elena Casarosa Andrea Ripoli Paolo Ghirri Antonio Boldrini Bruno Fink Andrea R Genazzani Flavio Coceani Tommaso Simoncini Compensatory feto-placental upregulation of the nitric oxide system during fetal growth restriction. PLoS ONE |
author_facet |
Silvia Pisaneschi Francesca A L Strigini Angel M Sanchez Silvia Begliuomini Elena Casarosa Andrea Ripoli Paolo Ghirri Antonio Boldrini Bruno Fink Andrea R Genazzani Flavio Coceani Tommaso Simoncini |
author_sort |
Silvia Pisaneschi |
title |
Compensatory feto-placental upregulation of the nitric oxide system during fetal growth restriction. |
title_short |
Compensatory feto-placental upregulation of the nitric oxide system during fetal growth restriction. |
title_full |
Compensatory feto-placental upregulation of the nitric oxide system during fetal growth restriction. |
title_fullStr |
Compensatory feto-placental upregulation of the nitric oxide system during fetal growth restriction. |
title_full_unstemmed |
Compensatory feto-placental upregulation of the nitric oxide system during fetal growth restriction. |
title_sort |
compensatory feto-placental upregulation of the nitric oxide system during fetal growth restriction. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2012-01-01 |
description |
<h4>Background</h4>Fetal Growth Restriction is often associated with a feto-placental vascular dysfunction conceivably involving endothelial cells. Our study aimed to verify this pathogenic role for feto-placental endothelial cells and, coincidentally, demonstrate any abnormality in the nitric oxide system.<h4>Methods</h4>Prenatal assessment of feto-placental vascular function was combined with measurement of nitric oxide (in the form of S-nitrosohemoglobin) and its nitrite byproduct, and of the endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine. Umbilical vein endothelial cells were also harvested to determine their gene profile. The study comprised term pregnancies with normal (n = 40) or small-for-gestational-age (n = 20) newborns, small-for-gestational-age preterm pregnancies (n = 15), and bi-chorial, bi-amniotic twin pregnancies with discordant fetal growth (n = 12).<h4>Results</h4>Umbilical blood nitrite (p<0.001) and S-nitrosohemoglobin (p = 0.02) rose with fetal growth restriction while asymmetric dimethylarginine decreased (p = 0.003). Nitrite rise coincided with an abnormal Doppler profile from umbilical arteries. Fetal growth restriction umbilical vein endothelial cells produced more nitrite and also exhibited reciprocal changes in vasodilator (upwards) and vasoconstrictor (downwards) transcripts. Elevation in blood nitrite and S-nitrosohemoglobin persisted postnatally in the fetal growth restriction offspring.<h4>Conclusion</h4>Fetal growth restriction is typified by increased nitric oxide production during pregnancy and after birth. This response is viewed as an adaptative event to sustain placental blood flow. However, its occurrence may modify the endothelial phenotype and may ultimately represent an element of risk for cardiovascular disease in adult life. |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23028913/pdf/?tool=EBI |
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