Korean J Obstet Gynecol.  2003 Feb;46(2):259-267.

Study on the Apoptosis and its Mediators in the Placentas of Preclampsia using cDNA Expression Array

• Choi WJ
• Choi WS
• Lee JH
• Paik WY

Abstract

OBJECTIVE
The present study was designed to examine whether preeclampsia is associated with an increase in placental apoptosis and to detect differential expression of mediators involved in apoptosis.
METHODS
Placental tissues from 10 cases of preeclampsia and 16 cases of control were analyzed using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) staining. And cDNA expression array assay was performed for detecting mediators that were involved in placental apoptosis.
RESULTS
In TUNEL staining, number of apoptotic nuclei were increased in placenta of preeclampsia. The expression of apoptotic signals was limited to trophoblasts. As a result of cDNA expression array assay, expressions of caspase-10, tumor necrosis factor receptor-1 (TNFR-1), and death domain receptor-3 (DDR-3) were increased and expression of cell division protein kinase-9 (CDK-9), cyclin A, insulin-like growth factor-1 (IGF-1), and insulin-like growth factor-binding protein-3 (IGFBP-3) were decreased in the placenta of preeclampsia. The expression of caspase-10, DDR-3, and IGFBP-3 between preeclampsia and normal revealed significantly different (p<0.05).
CONCLUSION
Apoptosis was significantly increased in placenta of preeclampsia and various mediators were involved in apoptotic mechanism. Therefore, it was suggested that apoptosis might play a role in the pathophysiologic mechanisms of preeclampsia.

Keyword

Apoptosis; Peclampsia; Placenta; cDNA expression array

MeSH Terms

Apoptosis*
Caspase 10
Cell Division
Cyclin A
Deoxyuridine
DNA, Complementary*
In Situ Nick-End Labeling
Insulin-Like Growth Factor Binding Protein 3
Placenta*
Pre-Eclampsia
Trophoblasts
Tumor Necrosis Factor-alpha
Caspase 10
Cyclin A
DNA, Complementary
Deoxyuridine
Insulin-Like Growth Factor Binding Protein 3
Tumor Necrosis Factor-alpha