Reduction of apoptosis and proliferation in endometriosis
Reduction of apoptosis and proliferation in endometriosis
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DOI：
10.1016/j.fertnstert.2003.11.048
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发表时间：
2004-07-01
影响因子：
6.7
通讯作者：
Foidart, JM
中科院分区：
文献类型：
--
作者：
Béliard, A;Noël, A;Foidart, JM
设计：免疫组织化学研究。地点：学术实验室。干预(S)：取自26-40岁因疼痛或不孕接受腹腔镜手术的妇女腹膜标本。主要结果(S)：采用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法(TUNEL)检测细胞凋亡。应用免疫组织化学方法检测30例子宫内膜异位症患者在位和异位内膜中P53、bcl2、雌孕激素(P)受体的表达及细胞增殖情况。结果：(S)：异位内膜病变以TUNEL和P53表达减弱，bcl2表达增强为特征。未发现细胞凋亡与雌激素受体和P受体水平的相关性。与在位内膜相比，异位内膜组织中类固醇受体的表达减少，无周期调节。结论：异位内膜组织与在位内膜在增殖率、激素水平及细胞凋亡标志物等方面存在差异。子宫内膜异位症细胞对凋亡敏感性的降低可能促进这些细胞向异位部位的扩散和植入。(C)2004年，由美国生殖医学会提供。
Objective: To evaluate whether endometriosis could be related to an impaired balance between apoptosis and proliferation, two processes which could be modulated by hormonal status.Design: Immunohistochemical study.Setting: Academic research laboratory.Intervention(s): Endometriotic samples obtained from peritoneum of women aged 26-40 years who were undergoing laparoscopy for pain or infertility.Main Outcome Measure(s): Apoptotic cells were detected with the use of the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. The production of p53 and bcl-2, estrogen and Progesterone (P) receptors, and cellular proliferation were assessed by immunohistochemistry in eutopic and ectopic endometria from 30 patients with endometriosis throughout the menstrual cycle. Results were compared with those from normal endometria from 15 fertile patients.Result(s): Endometriotic lesions were characterized by reduced TUNEL and p53 stainings and by enhanced bcl-2 staining. No correlation between apoptosis and estrogen receptor or P receptor levels was found. A lower amount of steroid receptor was found in endometriotic tissues, without cyclic modulation, compared with the eutopic endometrium.Conclusion(s): Our results suggest that when endometrial tissue is located at ectopic locations, it differs from eutopic endometrium by its proliferation rate, steroid hormone levels, and markers of apoptosis. A reduced sensitivity of endometriotic cells to apoptosis could promote the dissemination and implantation of these cells to ectopic sites. (C) 2004 by American Society for Reproductive Medicine.