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Open Access Highly Accessed Research

Intrauterine growth restriction and placental angiogenesis

Figen Barut1*, Aykut Barut2, Banu Dogan Gun1, Nilufer Onak Kandemir1, Mehmet Ibrahim Harma2, Muge Harma2, Erol Aktunc3 and Sukru Oguz Ozdamar1

Author affiliations

1 Department of Pathology, Faculty of Medicine, Zonguldak Karaelmas University, Zonguldak, Turkey

2 Department of Gynecology and Obstetrics, Faculty of Medicine, Zonguldak Karaelmas University, Zonguldak, Turkey

3 Department of Family Medicine, Faculty of Medicine, Zonguldak Karaelmas University, Zonguldak, Turkey

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Citation and License

Diagnostic Pathology 2010, 5:24  doi:10.1186/1746-1596-5-24

Published: 22 April 2010

Abstract

Background

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.

Methods

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.

Results

The expression of all the markers was significantly higher (p < 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.

Conclusion

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.