子宫内膜异位症和腺肌症患者子宫内膜雌激素受体的时空表达

目的　研究子宫内膜异位症和子宫腺肌症子宫内膜各种细胞中雌激素α和 β受体的表达模式 ,为探索子宫内膜异位症和子宫腺肌症的致病机理提供依据。　方法　 10 8例患有内膜异位症、腺肌症、两症并发组和对照组子宫内膜组织 ,常规光镜下按Noyes分期标准行形态学分期。采用免疫组织化学的方法观察不同月经周期时相子宫内膜腺上皮、基质和血管内皮细胞中雌激素受体ERα和ERβ的表达。　 结果　与对照组相比 ,ERα信号强度在各组相应的细胞类型、相应的时相无显著差异 ,但子宫内膜腺上皮细胞、基质细胞和血管内皮细胞中显示阳性信号的细胞比例增大 ,且腺上皮细胞质普遍出现ERα阳性信号。子宫内膜异位症和腺肌症的血管内皮细胞中ERα阳性细胞数显著增加。ERβ在各组的表达模式与对照组相比无明显差异 ,甚至略呈下降趋势。　结论　人子宫内膜中ERα为雌激素效应的主要受体亚型 ,表达ERα的腺上皮、基质和血管内皮细胞数量的增多以及腺上皮细胞质普遍出现ERα阳性信号可能与这两种疾病的发病密切相关 ;ERβ并不参与这一过程。

Temporal and spatial expression of estrogen receptor in the endometrium of patients with endometriosis,adenomyosis or both

Objective: For exploring the etiology of the endometriosis and adenomyosis, the expression patterns of estrogen receptor α and β in different cell types of endometrium in patients with endometriosis, adenomyosis or both during menstruation cycle were compared to the control endometrium. Methods: One hundred and eight endometrial samples were obtained from normal uterus as control, and from patients with endometriosis, adenomyosis or both by laparoscopy or hysterectomy. According to the Noyes’ dating criteria, the actually stages of endometrial samples were determined by H&E staining sections. The temporal and spatial expression of estrogen receptor α and β in the epithelial cells, stromal cells and endothelial cells of spiral artery in the eutopic endometrium from endometriosis, adenomyosis or both during menstruation cycle was compared to the normal endometrium by immunohistochemistry.Results: The expression intensity of ERα in endometrium of patients with endometriosis or adenomyosis was mostly parallel with that of normal endometrium. But the ERα positive signal frequency increased evidently either in glandular epithelial cells, or in stromal cells or in the vascular endothelial cells in the endometriosis and adenomyosis. The ERα positive signal occurred even more in the patient’s cytoplasm of glandular epithelial cells. The vascular endothelial cells with positive staining were arising mostly through out the menstrual cycle in the groups with endometriosis or adenomyosis. No significant difference was found in ERβ between the groups of patients and control. Conclusion: The regulatory effects of estrogen may be mediated mainly via ERα rather than ERβ in human endometrium. The elevation of signal frequency in glandular epithelial cells, stromal cells and vascular endothelial cells as well as the widespread expression of ERα in the cytoplasm of glandular epithelium may cause endometriosis and adenomyosis. ERβ might not be involved in the cause of endometriosis and adenomyosis.