Comparison of Placental Apoptosis in Normal Pregnancy, Preeclampsia and Intrauterine Growth Restriction / 대한산부인과학회잡지

ABSTRACT

OBJECTIVE: Aims of this study were to conclusively demonstrate apoptosis in the human placenta and to compare of placental apoptosis in normal pregnancy, preeclampsia and intrauterine growth restriction. METHODS: Placental samples obtained from 30 term, normal pregnancy, 30 pregnancies complicated intrauterine growth restriction, 30 pregnancies complicated preclampsia. The definition used to identify intrauterine growth restriction depends on fetal body weight ratio less than 10 percentile by ultrasonography. The definition used to identify preeclampsia depend on ACOG criteria. Light microscopy and polyclonal antibodies of Fas, Fas ligand, Bax, Bcl-2 were used to identify apoptosis. RESULTS: Apoptosis was conclusively demonstrated within placental tissue. Results of immunohis-tochemical analysis of Fas in the trophoblast of normal pregnancy, pregnancy induced hypertension and intrauterine growth restriction were negative of 86.7%, 26.7% and 13.3% respectively. Results of immunohistochemical analysis of Fas lgand in the trophoblast of normal pregnancy, pregnancy induced hypertension and intrauterine growth restriction were diffuse positive of 53.3%, 16.7% and 6.7% respectively. Results of immunohistochemical analysis of Bcl-2 in the trophoblast of normal pregnancy, pregnancy induced hypertension and intrauterine growth restriction were diffusely positive of 90.0%, 76.7% and 66.7% respectively. Results of immunohistochemical analysis of Bax in the trophoblast of normal pregnancy, preeclampsia and intrauterine growth restriction were diffuse positive of 40.0%, 40.0% and 50.0% respectively. CONCLUSION: Apoptosis and altered expression of Bcl-2 in trophoblast were conclusively demonstrated within placental tissue, suggesting that it may play a role in the normal development and aging of the placenta. Placental apoptosis and altered expression of Fas and Fas ligand in trophoblast might influence pathogenesis or pathophysiologic mechanism of preeclamsia and intrauterine growth restriction.