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Human trophoblast invasion and spiral artery transformation - The role of nitric oxide

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

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Abstract

During early human pregnancy extravillous cytotrophoblasts invade the uterus and also migrate up the spiral arteries, transforming them into large vessels of low resistance. Failure of transformation has been described in pre-eclampsia, fetal growth restriction, and miscarriage. Recent evidence suggests that some maternal vessels undergo structural changes without interaction with cytotrophoblasts. The possibility arises that local vasoactive mediators such as nitric oxide result in spiral artery dilatation before their invasion. In support of this, a recent histological study in the guinea pig suggested that cytotrophoblasts expressed nitric oxide synthase (NOS) as they surrounded vessels. This study tested the hypothesis that invading cytotrophoblasts express NOS and therefore have the potential to induce vasodilatation by releasing nitric oxide. The expression of NOS on extravillous cytotrophoblasts was studied in placental bed biopsies, obtained, using a transcervical sampling technique, from normal human pregnancies between 8 to 19 weeks of gestation and in the third trimester. Whereas eNOS was expressed by syncytiotrophoblast, neither eNOS or iNOS was expressed by extravillous cytotrophoblasts at any time during invasion. The mechanisms controlling spiral artery transformation are pivotal to understanding normal and abnormal placentation. These results suggest that trophoblast-derived nitric oxide is unlikely to contribute to spiral artery dilatation.


Publication metadata

Author(s): Bulmer JN; Robson SC; Lyall F; Kelly H; Duffie E

Publication type: Article

Publication status: Published

Journal: American Journal of Pathology

Year: 1999

Volume: 154

Issue: 4

Pages: 1105-1114

Print publication date: 01/04/1999

ISSN (print): 0002-9440

ISSN (electronic): 1525-2191

Publisher: Elsevier Inc.

URL: http://dx.doi.org/10.1016/S0002-9440(10)65363-1

DOI: 10.1016/S0002-9440(10)65363-1


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