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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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 |
work_keys_str_mv |
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