Immunolocalization of the Apoptotic Inhibiting Protein (bcl-2) in Early Normal Pregnancy and Abortion.
- Author:
Jiae LEE
1
;
Jeong Wook KIM
;
Bum Chae CHOI
;
Kwang Moon YANG
;
Young Youl CHO
;
Sung Ran HONG
Author Information
1. Laboratory of Reproductive Medicine, Samsung Cheil Hospital and Women's Healthcare Center, Sungkyunkwan University School of Medicine, Seoul 100-380, Korea. sungran@samsung.co.kr
- Publication Type:Original Article
- Keywords:
Pregnancy;
Missed abortion2;
Placenta;
Apoptosis;
bcl-2
- MeSH:
Abortion, Habitual;
Abortion, Missed;
Apoptosis;
Cell Proliferation;
Cell Survival;
Chorionic Villi;
Decidua;
Female;
Humans;
Immunohistochemistry;
Placenta;
Pregnancy Trimester, First;
Pregnancy*;
Proto-Oncogenes;
Trophoblasts
- From:Korean Journal of Pathology
2001;35(1):48-52
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The human placenta is an important organ in the maintenance of pregnancy, having functions in maturation and differentiation until the end of pregnancy. The bcl-2 protein is a proto-oncogene that prevents apoptosis and maintains cell survival. However, the mechanism through which bcl-2 inhibits apoptosis is unclear. The aims of this study are to localize bcl-2 at the placenta and to determine whether the expression of bcl-2 in early normal pregnancy is different from that of a missed abortion. METHODS: Immunohistochemistry was performed for bcl-2 in formalin-fixed chorionic villi and decidual tissue collected from five early normal pregnancies and eleven missed abortions having histories of recurrent abortions during the first trimester. RESULTS: The bcl-2 protein was observed in the syncytiotrophoblasts of chorionic villi and decidua in both the normal pregnancy and the missed abortion, and the expression of bcl-2 significantly increased in the missed abortion group (p<0.05). CONCLUSION: The bcl-2 may be necessary to maintain pregnancy through modulating the survival of the syncytiotrophoblast and decidua without affecting cell proliferation, and the increased bcl-2 expression is presumed to be a reparative process to the increased apoptotic activity.
