| Compensatory feto-placental upregulation of the nitric oxide system during fetal growth restriction. | |
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MedLine Citation:
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PMID: 23028913 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: 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. METHODS: 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). RESULTS: 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. CONCLUSION: 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. |
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Authors:
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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 |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2012-09-27 |
Journal Detail:
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Title: PloS one Volume: 7 ISSN: 1932-6203 ISO Abbreviation: PLoS ONE Publication Date: 2012 |
Date Detail:
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Created Date: 2012-10-02 Completed Date: 2013-02-28 Revised Date: 2013-03-01 |
Medline Journal Info:
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Nlm Unique ID: 101285081 Medline TA: PLoS One Country: United States |
Other Details:
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Languages: eng Pagination: e45294 Citation Subset: IM |
Affiliation:
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Division of Obstetrics and Gynecology, Department of Reproductive Medicine and Child Development, University of Pisa, Pisa, Italy. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Adaptation, Physiological Adult Arginine / analogs & derivatives*, blood Endothelial Cells / metabolism Endothelium, Vascular / metabolism, ultrasonography Female Fetal Blood / metabolism* Fetal Growth Retardation / blood*, genetics, ultrasonography Fetus Gene Expression Profiling Hemoglobins / metabolism Humans Infant, Low Birth Weight Infant, Newborn Nitric Oxide / biosynthesis* Nitric Oxide Synthase Type III / genetics, metabolism* Nitrites / blood Placenta / metabolism* Pregnancy Reverse Transcriptase Polymerase Chain Reaction Umbilical Arteries / metabolism, ultrasonography Umbilical Veins / metabolism, ultrasonography Up-Regulation |
| Chemical | |
Reg. No./Substance:
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0/Hemoglobins; 0/Nitrites; 0/S-nitrosohemoglobin; 10102-43-9/Nitric Oxide; 30315-93-6/N,N-dimethylarginine; 74-79-3/Arginine; EC 1.14.13.39/Nitric Oxide Synthase Type III |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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