Publication | Open Access
Preeclampsia is associated with abnormal expression of adhesion molecules by invasive cytotrophoblasts.
548
Citations
16
References
1993
Year
GynecologyPathologyCytoskeletonInvasive CytotrophoblastsImplantation (Embryology)Pregnancy Disorder PreeclampsiaAdhesion MoleculeNormal Human PregnancyPublic HealthPreeclampsiaPlacental DevelopmentAdhesion MoleculesMaternal HealthCell BiologyDevelopmental BiologyGestational HypertensionPregnancyEclampsiaMedicineAbnormal Expression
In normal pregnancy, cytotrophoblasts invade the uterus and arteries throughout the decidua and myometrium, accompanied by changes in adhesion molecule expression; in preeclampsia, invasion is restricted to superficial decidua with few arterioles breached. The study aimed to determine whether adhesion molecule expression by cytotrophoblasts is also abnormal in preeclampsia. Placental bed biopsies from normal and preeclamptic pregnancies were stained with anti‑integrin antibodies to assess adhesion molecule expression. The study found that adhesion molecule switching is abnormal in preeclampsia, indicating a failure of trophoblast differentiation and a shift toward adhesive interactions that restrain invasion, resulting in shallow uterine invasion.
In normal human pregnancy, invasion of the uterus and its arterial system by cytotrophoblasts extends through the entire decidua and the adjacent third of the myometrium. Our previous work showed that during the first trimester of pregnancy, invasion is accompanied by a marked change in the expression of cell adhesion molecules by invasive cytotrophoblasts. In the pregnancy disorder preeclampsia, cytotrophoblast invasion is limited to the superficial decidua, and few arterioles are breached. The purpose of this study was to determine whether cytotrophoblast expression of adhesion molecules in this disorder is also abnormal. Placental bed biopsy specimens from normal pregnancies and those complicated by preeclampsia were stained with anti-integrin antibodies. The results showed that adhesion molecule switching by invasive cytotrophoblasts is abnormal in preeclampsia, which suggests that this subpopulation of trophoblast cells fails to differentiate properly. A likely result is that the delicate balance of adhesive interactions that normally permit cytotrophoblast invasion is tipped in favor of those which restrain this process, with the net effect of shallow uterine invasion.
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