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Transforming growth factor-beta expression in human placenta and placental bed in third trimester normal pregnancy, preeclampsia, and fetal growth restriction

Lookup NU author(s): Dr Judith Bulmer, Professor Steve Robson

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Abstract

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)-beta3 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-betas 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-beta1, TGF-beta2, and TGF-beta3 in placenta and placental bed of pregnancies complicated by PE and FGR and matched control pregnancies. The results show that TGF-beta1, -beta2, and -beta3 are not expressed in villous trophoblasts but are present within the placenta. TGF-beta1, -beta2, and, to a much lesser extent, TGF-beta3 were present within the placental bed but only TGF-beta2 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-beta3 being responsible for failed trophoblast invasion in PE. Our findings suggest that the TGF-betas do not have a pathophysiological role in either PE or FGR.


Publication metadata

Author(s): Bulmer JN; Robson SC; Lyall F; Simpson H; Barber A

Publication type: Article

Publication status: Published

Journal: American Journal of Pathology

Year: 2001

Volume: 159

Issue: 5

Pages: 1827-1838

Print publication date: 21/12/2010

ISSN (print): 0002-9440

ISSN (electronic): 1525-2191

Publisher: Elsevier Inc.

URL: http://dx.doi.org/10.1016/S0002-9440(10)63029-5

DOI: 10.1016/S0002-9440(10)63029-5


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