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Title: Immunohistochemical localization of endothelin-1 in human placenta from normal and growth-restricted pregnancies. Author: Erdem M, Erdem A, Erdem O, Yildirim G, Memis L, Himmetoğlu O. Journal: Pediatr Dev Pathol; 2003; 6(4):307-13. PubMed ID: 14692644. Abstract: The purpose of this study was to investigate whether the localization of endothelin-1 (ET-1) immunoreactivity differs in human placental tissues from third-trimester normal and intrauterine growth restricted (IUGR) pregnancies. Immunohistochemistry for ET-1 was performed on human placentas from 30 IUGR and 30 uncomplicated pregnancies matched for gestational age. The distribution and intensity of ET-1 immunoreactivity was assessed by a semiquantitative scoring system. Doppler flow velocity waveform analysis of the umbilical artery was performed in each patient before delivery. ET-1 was localized diffusely in placental specimens from normal and IUGR pregnancies. The localization of ET-1 immunoreactivity was significantly higher in the capillary endothelial cells of villi as well as in the endothelial, decidual, and trophoblastic cells of the basal plate in placentas from normal pregnancies than from IUGR pregnancies. There was no significant difference in placental ET-1 immunoreactivity between IUGR pregnancies with normal and abnormal umbilical artery Doppler flow velocity waveforms. Placental ET-1 immunoreactivity was significantly higher in the decidual and trophoblastic cells of the basal plate and the capillary endothelial cells of villi in normal pregnancies than in IUGR pregnancies with normal umbilical artery Doppler flow velocity waveforms. However, only the decidual and trophoblastic cells of the basal plate demonstrated significantly higher abundant localization of ET-1 immunoreactivity in normal pregnancies than in IUGR pregnancies with abnormal umbilical artery Doppler flow velocity waveforms. In conclusion, our findings suggest that the lower expression of ET-1 in placental tissues from IUGR pregnancies might be secondary to an adaptive mechanism to reduce the vasoconstrictor effect of ET-1.[Abstract] [Full Text] [Related] [New Search]