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(American Journal of Pathology. 2001;159:1827-1838.)
© 2001 American Society for Investigative Pathology

Regular Articles

Transforming Growth Factor-ß Expression in Human Placenta and Placental Bed in Third Trimester Normal Pregnancy, Preeclampsia, and Fetal Growth Restriction

Fiona Lyall*, Helen Simpson{dagger}, Judith Nicola Bulmer{ddagger}, Andrew Barber* and Stephen Courtenay Robson{dagger}

From the Maternal and Fetal Medicine Section,*
Institute of Medical Genetics, University of Glasgow, Yorkhill, Glasgow; and the Departments of Obstetrics and Gynaecology,{dagger}
and Pathology,{ddagger}
University of Newcastle upon Tyne, Royal Victoria Infirmary, Newcastle-upon-Tyne, United Kingdom

Normal human pregnancy depends on physiological transformation of spiral arteries by invasive trophoblasts. Preeclampsia (PE) and fetal growth restriction (FGR) are associated with impaired trophoblast invasion and spiral artery transformation. Recent studies have suggested that transforming growth factor (TGF)-ß3 is overexpressed in the placenta of PE patients and that this may be responsible for failed trophoblast invasion. There are, however, no studies on TGF-ßs in the placenta in FGR or in the placental bed in PE or FGR. In this study we have used immunohistochemistry, Western blot analysis, and enzyme-linked immunosorbent assay to examine the expression of TGF-ß1, TGF-ß2, and TGF-ß3 in placenta and placental bed of pregnancies complicated by PE and FGR and matched control pregnancies. The results show that TGF-ß1, -ß2, and -ß3 are not expressed in villous trophoblasts but are present within the placenta. TGF-ß1, -ß2, and, to a much lesser extent, TGF-ß3 were present within the placental bed but only TGF-ß2 was present in extravillous trophoblast. No changes in expression of either isoform were found in placenta or placental bed in PE or FGR compared with normal pregnancy. These data are not consistent with overexpression of TGF-ß3 being responsible for failed trophoblast invasion in PE. Our findings suggest that the TGF-ßs do not have a pathophysiological role in either PE or FGR.




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