Okulicz W C, Ace C I, Scarrell R
Department of Obstetrics and Gynecology, University of Massachusetts Medical School, Worcester 01655, USA.
Proc Soc Exp Biol Med. 1997 Feb;214(2):132-8. doi: 10.3181/00379727-214-44079.
The objective of the present study was to examine the zonal changes in endometrial proliferation that occur during the late secretory phase, menses, and postmenstrual endometrial regeneration. We used as our model ovariectomized rhesus monkey in which artificial menstrual cycles were simulated. Our marker of proliferation was the immunohistochemical detection of the Ki-67 antigen. On Day 26, as progesterone (P) levels are falling in the late secretory phase, proliferation in zone IV of the basalis decreased compared with Day 23 (peak P level). Proliferation in the upper regions of the endometrium remained suppressed. Three days after a single bolus injection of the potent antiprogestin RU-486 on Day 20, proliferation in zone IV was virtually absent compared with Day 23 of an artificial cycle. No distinct changes in the pattern of proliferation were observed in the upper regions of the endometrium. On Day 1 of menses (P levels undetectable, estradiol [E] levels of 70-100 pg/ml), there was little proliferation throughout the endometrium. On Day 3 or menses, proliferation returned to zones II-III of the basalis and the functionalis. This proliferation was primarily observed in the glandular epithelia whereas little or no proliferation was observed in zone IV of the basalis. By Day 5 proliferation continued in the glandular epithelia of zones I, II, and III, and was now clearly observable in the stromal cells. Only minimal proliferation was observed in glandular epithelia of zone IV. In the absence of basal E stimulation the return of proliferation to the glandular epithelia in zones I, II, and III was dramatically reduced. These data demonstrate a reciprocal pattern of proliferation in glandular epithelia that is dependent on the prevailing hormonal stimulation. Under P dominance, proliferation is inhibited in zones I, II, and III, and maintained in zone IV, whereas under E dominance (Day 3 or 5) proliferation is driven by E stimulation in zones I, II, and III with little or no proliferation present in zone IV. In addition, the inhibition of proliferation in zone IV by the antiprogestin RU-486 and the decline of zone IV proliferation associated with falling P levels provide further evidence that proliferation of glandular epithelia in zone IV is mediated in part by P.
本研究的目的是研究在分泌晚期、月经期和月经后子宫内膜再生过程中子宫内膜增殖的区域变化。我们使用模拟人工月经周期的去卵巢恒河猴作为模型。我们的增殖标志物是Ki-67抗原的免疫组化检测。在第26天，随着分泌晚期孕酮（P）水平下降，基底层IV区的增殖与第23天（P水平峰值）相比有所减少。子宫内膜上部区域的增殖仍受到抑制。在第20天单次推注强效抗孕激素RU-486三天后，与人工周期的第23天相比，IV区几乎没有增殖。在子宫内膜上部区域未观察到增殖模式的明显变化。在月经第1天（P水平不可检测，雌二醇[E]水平为70-100 pg/ml），整个子宫内膜几乎没有增殖。在月经第3天，增殖恢复到基底层和功能层的II-III区。这种增殖主要在腺上皮中观察到，而在基底层IV区几乎没有或没有增殖。到第5天，I、II和III区的腺上皮中增殖仍在继续，现在在基质细胞中也清晰可见。IV区的腺上皮中仅观察到极少的增殖。在没有基底E刺激的情况下，I、II和III区腺上皮中增殖的恢复显著减少。这些数据表明，腺上皮中的增殖呈现相互对应的模式，这取决于当时的激素刺激。在P占主导时，I、II和III区的增殖受到抑制，而IV区保持增殖，而在E占主导时（第3天或第5天），I、II和III区的增殖由E刺激驱动，IV区几乎没有或没有增殖。此外，抗孕激素RU-486对IV区增殖的抑制以及与P水平下降相关的IV区增殖减少进一步证明，IV区腺上皮的增殖部分由P介导。
