Differences in Apoptotic Susceptibility of Cytotrophoblasts and Syncytiotrophoblasts in Normal Pregnancy to Those Complicated with Preeclampsia and Intrauterine Growth Restriction

Differences in Apoptotic Susceptibility of Cytotrophoblasts and Syncytiotrophoblasts in Normal Pregnancy to Those Complicated with Preeclampsia and Intrauterine Growth Restriction

Placental apoptosis is increased in vivo in preeclampsia (PE) and intrauterine growth restriction (IUGR). The cause and pathological implications of this phenomenon are unknown. This study considers the apoptotic susceptibility of villous trophoblasts from normal, PE, and IUGR pregnancies. Cultured...

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Veröffentlicht in:The American journal of pathology 2003-02, Vol.162 (2), p.637-643
Hauptverfasser: Crocker, Ian P., Cooper, Suzanne, Ong, Stephen C., Baker, Philip N.
Format: Artikel
Sprache:eng
Schlagworte:
Adenosine Diphosphate - metabolism
Adenosine Triphosphate - metabolism
Adult
Annexin A5 - metabolism
Apoptosis
Biological and medical sciences
Cells, Cultured
Chorionic Gonadotropin - analysis
Diseases of mother, fetus and pregnancy
Female
Fetal Growth Retardation - pathology
Gynecology. Andrology. Obstetrics
Humans
In Situ Nick-End Labeling
Interferon-gamma - pharmacology
Maternal Age
Medical sciences
Middle Aged
Models, Biological
Oxygen Consumption - drug effects
Parity
Pre-Eclampsia - pathology
Pregnancy - physiology
Pregnancy. Fetus. Placenta
Regular
Trophoblasts - classification
Trophoblasts - cytology
Trophoblasts - pathology
Tumor Necrosis Factor-alpha - pharmacology
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Zusammenfassung:Placental apoptosis is increased in vivo in preeclampsia (PE) and intrauterine growth restriction (IUGR). The cause and pathological implications of this phenomenon are unknown. This study considers the apoptotic susceptibility of villous trophoblasts from normal, PE, and IUGR pregnancies. Cultured cytotrophoblasts (CTs) and an in vitro model of syncytialization were used. CTs were isolated from term placentas of 12 normal, 12 PE, and 12 IUGR pregnancies. Apoptosis was determined by terminal dUTP nick-end labeling (TUNEL), Annexin V binding, and ADP:ATP ratios. Cells were stimulated with tumor necrosis factor-α/interferon-γ or reduced oxygen (
ISSN:0002-9440
1525-2191
DOI:10.1016/S0002-9440(10)63857-6