Human trophoblast invasion and spiral artery transformation: the role of nitric oxide.
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.
Lyall
F
F
Maternal and Fetal Medicine Section, Institute of Medical Genetics, University of Glasgow, Yorkhill, Glasgow, United Kingdom. f.lyall@udcf.gla.ac.uk
Bulmer
J N
JN
Kelly
H
H
Duffie
E
E
Robson
S C
SC
D001158:Arteries / Q000502:physiology*; D015153:Blotting, Western; D004591:Electrophoresis, Polyacrylamide Gel; D005260:Female; D005865:Gestational Age; D006801:Humans; D007150:Immunohistochemistry; D007633:Keratins / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; D010920:Placenta / Q000098:blood supply / Q000201:enzymology*; D011247:Pregnancy; D014327:Trophoblasts / Q000166:cytology / Q000201:enzymology*; D014599:Uterus / Q000098:blood supply*; D014664:Vasodilation
D009569:Nitric Oxide; D007633:Keratins; C496319:NOS2 protein, human; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III