The comparison of endogenous angiogenesis inhibitors in normotensive and preeclamptic placentas: an immunohistochemical study

Abstract

Objective: Recently, it has been reported that endogenous angiogenesis inhibitors play a key role in the pathophysiology of preeclampsia. Thrombospondin-1, angiostatin and vasostatin are endogenous angiogenesis inhibitors and so far have not been shown in placenta at the immunohistochemical level. The aim of this study was to compare staining patterns of these endogenous angiogenesis inhibitors immunohistochemically in placentas of preeclamptic and normotensive pregnant women. Methods: Into the study, placentas from 20 preeclamptic and 20 normotensive pregnant women were included. Central and peripheral tissues were taken from both sides of placentas. Paraffin tissue blocks were prepared and stained for immunohistochemical analysis. Slides were evaluated for syncytiotrophoblasts, cytotrophoblasts, extra-villous throphoblasts and decidual cells. The degree of staining of slides were classified as negative, weak, moderate and strong. Results: Samples from preeclamptic patients were compared with those of normotensive. Staining of thrombospondin-1 was observed to increase in decidual cells, syncytiotrophoblasts in chorionic and stem villi and stroma of stem villi. Increased staining of thrombospondin-1 was only significant in the amniotic epithelium of the central sections. In addition, increased staining intensity of angiostatin was detected in the amniotic epithelium and chorionic plate of central sections of placenta. In peripheral sections, staining of angiostatin also increased in decidual cells but decreased in chorionic plate. Vasostatin staining in decidual cells, decidual stroma and chorionic villous stroma from peripheral sections decreased, but any difference was not observed in the central sections. Conclusion: Our results suggest that thrombospondin-1, angiostatin and vasostatin may play a role in the pathophysiology of preeclampsia. Further molecular studies are required to understand this role.

• Angiogenesis
• Angiostatin
• Placenta
• Preeclampsia
• Thrombospondin-1
• Vasostatin

Acknowledgements

We thank to Dr Nihat Nermutluoglu for his kind contribution to this work.