Trophoblastic remodeling in normal and preeclamptic pregnancies: implication of cytokines.
OBJECTIVE
To summarize the recent knowledge on the implications of placenta and cytokines in normal and preeclamptic pregnancies.


METHODS
A literature search was conducted of applicable articles related to interactions between trophoblast and cytokines in generating preeclampsia.


CONCLUSIONS
The initiating event in preeclampsia has been postulated to be the reduced uteroplacental perfusion as a result of abnormal extravillous cytotrophoblast invasion and remodeling of the uterine spiral arteries. Focal ischemia and hypoxia, deportation of hypoxemic trophoblast cells and abnormal expression of various placental biologic molecules, particularly the cytokines, are thought to lead to widespread dysfunction of the maternal vascular endothelium resulting in overproduction of endothelin and thromboxane, enhanced vascular sensitivity to angiotensin II, and reduced secretion of vasodilators such as nitric oxide and prostacyclin. These alterations, in turn, cause hypertension, proteinuria and edema, and pathologies in many organ systems (kidney, lung, liver, brain).
Kharfi
Abdelaziz
A
Unité de périnatalogie, Centre de Recherche de l'Hôpital Saint-François d'Assise, CHUQ, Québec, Canada.
Giguère
Yves
Y
Sapin
Vincent
V
Massé
Jacques
J
Dastugue
Bernard
B
Forest
Jean-Claude
JC
D016207:Cytokines / Q000502:physiology; D005260:Female; D006801:Humans; D010920:Placenta / Q000502:physiology / Q000503:physiopathology; D011225:Pre-Eclampsia / Q000503:physiopathology*; D011247:Pregnancy; D014327:Trophoblasts / Q000502:physiology*
D016207:Cytokines