초기 정상임신과 계류유산에서의 세포자멸사 억제인자 (bcl-2)의 발현
Immunolocalization of the Apoptotic Inhibiting Protein (bcl-2) in Early Normal Pregnancy and Abortion
이지애, 김정욱, 최범채, 양광문, 조영열, 홍성란,
소속 상세정보
이지애 ( Lee Ji-Ae )
성균관대학교 의과대학 삼성제일병원 불임연구실
김정욱 ( Kim Jeong-Wook )
성균관대학교 의과대학 삼성제일병원 불임연구실
최범채 ( Choi Bum-Chae )
성균관대학교 의과대학 삼성제일병원 산부인과
양광문 ( Yang Kwang-Moon )
성균관대학교 의과대학 삼성제일병원 산부인과
조영열 ( Cho Young-Youl )
조산부인과의원
홍성란 ( Hong Sung-Ran )
성균관대학교 의과대학 삼성제일병원 조직병리과
KMID : 0357920010350010048
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.
키워드
Pregnancy;Missed abortion;Placenta;Apoptosis;bcl-2
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