Intrauterine growth restriction and placental angiogenesis

<p>Abstract</p> <p>Background</p> <p>Vascular endothelial growth factor (VEGF), basic-fibroblast growth factor (b-FGF), and endothelial nitric oxide synthase (eNOS) are factors that take part in placental angiogenesis. They are highly expressed during embryonic and feta...

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Main Authors: Harma Muge, Harma Mehmet, Kandemir Nilufer, Gun Banu, Barut Aykut, Barut Figen, Aktunc Erol, Ozdamar Sukru
Format: Article
Language:English
Published: BMC 2010-04-01
Series:Diagnostic Pathology
Online Access:http://www.diagnosticpathology.org/content/5/1/24
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spelling doaj-8f3c309be0cb4854b404d8024b274e3a2020-11-25T01:31:58ZengBMCDiagnostic Pathology1746-15962010-04-01512410.1186/1746-1596-5-24Intrauterine growth restriction and placental angiogenesisHarma MugeHarma MehmetKandemir NiluferGun BanuBarut AykutBarut FigenAktunc ErolOzdamar Sukru<p>Abstract</p> <p>Background</p> <p>Vascular endothelial growth factor (VEGF), basic-fibroblast growth factor (b-FGF), and endothelial nitric oxide synthase (eNOS) are factors that take part in placental angiogenesis. They are highly expressed during embryonic and fetal development, especially in the first trimester. In this study, we aimed to investigate the role of placental angiogenesis in the development of intrauterine growth restriction (IUGR) by comparing the levels of expression of VEGF-A, b-FGF, and eNOS in normal-term pregnancy and IUGR placentas.</p> <p>Methods</p> <p>The expression of VEGF-A, b-FGF, and eNOS was studied using the avidin-biotin-peroxidase method in placental tissues diagnosed as normal (n = 55) and IUGR (n = 55). Results were evaluated in a semi-quantitative manner.</p> <p>Results</p> <p>The expression of all the markers was significantly higher (<it>p </it>< 0.001) in cytotrophoblasts, syncytiotrophoblasts, extravillous trophoblasts, vascular smooth muscle cells, chorionic villous stromal cells, and villous vascular endothelial cells of the IUGR placentas when compared with those collected from normal-term pregnancies.</p> <p>Conclusion</p> <p>Increased expression of VEGF-A, b-FGF, and eNOS may be the result of inadequate uteroplacental perfusion, supporting the proposal that abnormal angiogenesis plays a role in the pathophysiology of IUGR.</p> http://www.diagnosticpathology.org/content/5/1/24
collection DOAJ
language English
format Article
sources DOAJ
author Harma Muge
Harma Mehmet
Kandemir Nilufer
Gun Banu
Barut Aykut
Barut Figen
Aktunc Erol
Ozdamar Sukru
spellingShingle Harma Muge
Harma Mehmet
Kandemir Nilufer
Gun Banu
Barut Aykut
Barut Figen
Aktunc Erol
Ozdamar Sukru
Intrauterine growth restriction and placental angiogenesis
Diagnostic Pathology
author_facet Harma Muge
Harma Mehmet
Kandemir Nilufer
Gun Banu
Barut Aykut
Barut Figen
Aktunc Erol
Ozdamar Sukru
author_sort Harma Muge
title Intrauterine growth restriction and placental angiogenesis
title_short Intrauterine growth restriction and placental angiogenesis
title_full Intrauterine growth restriction and placental angiogenesis
title_fullStr Intrauterine growth restriction and placental angiogenesis
title_full_unstemmed Intrauterine growth restriction and placental angiogenesis
title_sort intrauterine growth restriction and placental angiogenesis
publisher BMC
series Diagnostic Pathology
issn 1746-1596
publishDate 2010-04-01
description <p>Abstract</p> <p>Background</p> <p>Vascular endothelial growth factor (VEGF), basic-fibroblast growth factor (b-FGF), and endothelial nitric oxide synthase (eNOS) are factors that take part in placental angiogenesis. They are highly expressed during embryonic and fetal development, especially in the first trimester. In this study, we aimed to investigate the role of placental angiogenesis in the development of intrauterine growth restriction (IUGR) by comparing the levels of expression of VEGF-A, b-FGF, and eNOS in normal-term pregnancy and IUGR placentas.</p> <p>Methods</p> <p>The expression of VEGF-A, b-FGF, and eNOS was studied using the avidin-biotin-peroxidase method in placental tissues diagnosed as normal (n = 55) and IUGR (n = 55). Results were evaluated in a semi-quantitative manner.</p> <p>Results</p> <p>The expression of all the markers was significantly higher (<it>p </it>< 0.001) in cytotrophoblasts, syncytiotrophoblasts, extravillous trophoblasts, vascular smooth muscle cells, chorionic villous stromal cells, and villous vascular endothelial cells of the IUGR placentas when compared with those collected from normal-term pregnancies.</p> <p>Conclusion</p> <p>Increased expression of VEGF-A, b-FGF, and eNOS may be the result of inadequate uteroplacental perfusion, supporting the proposal that abnormal angiogenesis plays a role in the pathophysiology of IUGR.</p>
url http://www.diagnosticpathology.org/content/5/1/24
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AT harmamehmet intrauterinegrowthrestrictionandplacentalangiogenesis
AT kandemirnilufer intrauterinegrowthrestrictionandplacentalangiogenesis
AT gunbanu intrauterinegrowthrestrictionandplacentalangiogenesis
AT barutaykut intrauterinegrowthrestrictionandplacentalangiogenesis
AT barutfigen intrauterinegrowthrestrictionandplacentalangiogenesis
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