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

Citation
F. Lyall et al., Transforming growth factor-beta expression in human placenta and placentalbed in third trimester normal pregnancy, preeclampsia, and fetal growth restriction, AM J PATH, 159(5), 2001, pp. 1827-1838
Citations number
65
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
AMERICAN JOURNAL OF PATHOLOGY
ISSN journal
00029440 → ACNP
Volume
159
Issue
5
Year of publication
2001
Pages
1827 - 1838
Database
ISI
SICI code
0002-9440(200111)159:5<1827:TGFEIH>2.0.ZU;2-M
Abstract
Normal human pregnancy depends on physiological transformation of spiral ar teries by invasive trophoblasts. Preeclampsia (PE) and fetal growth restric tion (FGR) are associated with impaired trophoblast invasion and spiral art ery 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, howeve r, no studies on TGF-betas in the placenta in FGR or in the placental bed i n PE or FGR. In this study we have used immunohistochemistry, Western blot analysis, and enzyme-linked immunosorbent assay to examine the expression o f TGF-beta1, TGF-beta2, and TGF-beta3 in placenta and placental bed of preg nancies complicated by PE and FGR and matched control pregnancies. The resu lts show that TGF-beta1, -beta2, and -beta3 are not expressed in villous tr ophoblasts but are present within the placenta. TGF-beta1, -beta2, and, to a much lesser extent, TGF-beta3 were present within the placental bed but o nly TGF-beta2 was present in extravillous trophoblast. No changes in expres sion of either isoform were found in placenta or placental bed in PE or FGR compared with normal pregnancy. These data are not consistent with overexp ression of TGF-beta3 being responsible for failed trophoblast invasion in P E. Our findings suggest that the TGF-betas do not have a pathophysiological role in either PE or FGR.