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Intrauterine growth restriction and placental angiogenesis.

Barut F, Barut A, Gun BD, Kandemir NO, Harma MI, Harma M, Aktunc E, Ozdamar SO - Diagn Pathol (2010)

Bottom Line: They are highly expressed during embryonic and fetal development, especially in the first trimester.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.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pathology, Faculty of Medicine, Zonguldak Karaelmas University, Zonguldak, Turkey. figenbarut@yahoo.com

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.

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Related in: MedlinePlus

b-FGF expression in placental tissues, A; Normal placental villous displaying weak b-FGF immune reaction, B; Strong b-FGF expression in IUGR placenta (B-SA peroxidase, DAB, A; B; ×200).
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Figure 3: b-FGF expression in placental tissues, A; Normal placental villous displaying weak b-FGF immune reaction, B; Strong b-FGF expression in IUGR placenta (B-SA peroxidase, DAB, A; B; ×200).

Mentions: In normal term pregnancy placentas, staining was weak and located predominantly in the cytotrophoblasts and syncytiotrophoblasts (Fig. 2A, 3A, 4A). In IUGR placentas, strong staining was obtained with VEGF-A (Fig. 2B), b-FGF (Fig. 3B), and eNOS (Fig. 4B) primary antibodies.


Intrauterine growth restriction and placental angiogenesis.

Barut F, Barut A, Gun BD, Kandemir NO, Harma MI, Harma M, Aktunc E, Ozdamar SO - Diagn Pathol (2010)

b-FGF expression in placental tissues, A; Normal placental villous displaying weak b-FGF immune reaction, B; Strong b-FGF expression in IUGR placenta (B-SA peroxidase, DAB, A; B; ×200).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2865442&req=5

Figure 3: b-FGF expression in placental tissues, A; Normal placental villous displaying weak b-FGF immune reaction, B; Strong b-FGF expression in IUGR placenta (B-SA peroxidase, DAB, A; B; ×200).
Mentions: In normal term pregnancy placentas, staining was weak and located predominantly in the cytotrophoblasts and syncytiotrophoblasts (Fig. 2A, 3A, 4A). In IUGR placentas, strong staining was obtained with VEGF-A (Fig. 2B), b-FGF (Fig. 3B), and eNOS (Fig. 4B) primary antibodies.

Bottom Line: They are highly expressed during embryonic and fetal development, especially in the first trimester.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.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pathology, Faculty of Medicine, Zonguldak Karaelmas University, Zonguldak, Turkey. figenbarut@yahoo.com

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.

Show MeSH
Related in: MedlinePlus