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Human trophoblast invasion and spiral artery transformation - The role of PECAM-1 in normal pregnancy, preeclampsia, and fetal growth restriction

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


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During early human pregnancy extravillous cytotrophoblasts invade the uterus and spiral arteries transforming them into large vessels of low resistance, Failure of trophoblast invasion and spiral artery transformation occurs in preeclampsia and fetal growth restriction (FGR); these processes are not well understood. Recent studies have suggested that cytotrophoblasts that invade spiral arteries mimic the endothelial cells they replace and express PECAM-1. It was also reported that in preeclampsia, cytotrophoblasts fail to express PECAM-1 and that failure to express endothelial cell adhesion molecules may account for failed trophoblast invasion. Despite the possible importance of adhesion molecules in trophoblast invasion, no study has systematically investigated the expression of PECAM-1 in the placental bed throughout the period of invasion, particularly in the myometrial segments where the key failure occurs. There are no studies on PECAM-1 expression in the placental bed in FGR, We have examined the expression of PECAM-1 in placental bed biopsies and placentas from 8 to 19 weeks Of gestation and in the placenta and placental bed in the third trimester in cases of preeclampsia, FGR, and control pregnancies. PECAM-1 was expressed on endothelium of vessels in the placenta and placental bed but not by villous or extravillous trophoblasts in normal or pathological samples. These findings do not support a role for PECAM-1 in normal invasion or in the pathophysiology of preeclampsia or FGR.

Publication metadata

Author(s): Bulmer JN; Robson SC; Lyall F; Duffie E; Cousins F; Theriault A

Publication type: Article

Publication status: Published

Journal: American Journal of Pathology

Year: 2001

Volume: 158

Issue: 5

Pages: 1713-1721

Print publication date: 21/12/2010

ISSN (print): 0002-9440

ISSN (electronic): 1525-2191

Publisher: Elsevier Inc.


DOI: 10.1016/S0002-9440(10)64127-2


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