The immunohistochemically comparison of endogenous angiogenesis inhibitors in preeclamptic and normotensive placentas

Preeclampsia is a pregnancy-specific hypertensive disorder stemming from placenta, and systemic s syndrome characterized with widespread maternal endotelial dysfunction. Recently, it has been reported that antiangiogenetics play a key role in the etiology of preeclampsia pathophysiology. The aim of this study is to immunohistochemically compare the expressions of such antiangiogenetics in preeclamptic and normtensive placentas, as thrombospondin-1, angiostatin, and vasostatin the efficacy of which have not been established earlier in preeclampsia.In the study, 20 preeclamptic and 20 normotensive (control) pregnant placenta were used. From maternal and fetal parts of the placentas, two tissue sections of 1×1 cm3 were taken: one from periphery and the other from central. Then rutin paraffin tissue blokcs were performed. The sections taken from paraffin blokcs were stained with H-E, Trichrom Masson, PAS for histochemical analysis, and with Thrombospondin-1, Angiostatin and Vasostatin for histopathologic evaluation.In histopathologic analysis of preeclamptic placenta, perivillouse fibrin accumulation, increase in intervillose interval, sintitial knot increase, thickening in basal membran, capillary dilatations and obliteration in vessel lumen were determined. While the expression of thrombospondin-1, which is an antiogenic molecule of matrix derived, occurred in almost all of the placenta, this expression which is often observed in syncytotrophoblast and decidual cells, was observed to have increased in preeclamptics. Although angiostatin, which is an antiangiogenic molecule of non-matrix origin, was expressed in sintitial knots and bridges, no difference was found between the two groups. In vasostatin, however, immun reaction was observed in decidual cells, decidual stroma and syncytotrophoblast cells. When, the groups were compared in this respect, any difference was not found.In conclusion, of anti angiogenic agents, thrombospondin-1, angiostatin and vasostatin played a part in pathophsiology of preeclampsia; however, the most important of these were thrombospondin-1 and angiostatin. Decidual cells were involved most, in the center of these molecules effects.