The expression of apoptosis-related proteins Bcl-2 and Ki67 in endometrium of ovulatory menstrual cycles

被引:64
作者
Mertens, HJMM
Heineman, MJ
Evers, JLH
机构
[1] Univ Hosp Maastricht, Res Inst Growth & Dev, Maaslandzienkenhuis Sittard, Dept Obstet & Gynecol, NL-6131 BK Sittard, Netherlands
[2] Acad Hosp Groningen, Dept Obstet & Gynecol, Groningen, Netherlands
关键词
apoptosis; Bcl-2; Ki67; endometrium; tissue remodeling;
D O I
10.1159/000064569
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Background. During the menstrual cycle, a rapid sequence of proliferation, differentiation and cell death occurs in the human endometrium. Mechanisms involved in cell proliferation have been studied extensively. Apoptosis has recently been recognized to be a physiologic phenomenon. The aim of this study was to investigate the mechanisms involved in hormone-dependent tissue remodeling by measuring Bcl-2, an apoptosis inhibitor, and Ki67, a proliferation marker, as expressed in normal human endometrium. Methods: Paraffin-embedded endometrial sections of 30 uteri were immunostained for Bcl-2 and Ki67; expression was scored in cavitary epithelium, functional and basal glandular epithelial and stromal cells of the endometrium. Results: Bcl-2 expression increased in the proliferative phases and decreased significantly in the secretory phases, especially in glandular epithelial cells (131 +/- 45 for functional laminal cells and 227 +/- 68 for basal laminal cells to 0). Ki67 expression showed the same cyclic pattern with a later onset (145 +/- 63 for functional laminal cells and 13 +/- 8 for basal laminal cells to 0). Conclusion: Bcl-2 promotes cell survival by preventing apoptosis. Proliferation is the result of increasing estradiol concentration, high estrogen receptor expression and growth hormones and high Bcl-2 and Ki67 expression. After the onset of progesterone production, Bcl-2 levels decrease and Ki67 levels and androgen receptor expression in stromal cells disappear resulting in cell disintegration and menstruation. Persistent Bcl-2 expression, like we saw in basal laminal stromal and epithelial cells, accounts for the privilege of escaping from apoptosis-inducing signals. This allows reconstruction of the functional endometrium from its preserved basal layer after menstruation. Copyright (C) 2002 S. Karger AG, Basel.
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页码:224 / 230
页数:7
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