Department of Surgical Sciences, University of Udine, 33100 Udine, Italy.
Hum Reprod. 2011 Oct;26(10):2731-41. doi: 10.1093/humrep/der264. Epub 2011 Aug 12.
The roles of cell proliferation and genomic instability in endometriosis are highly debated aspects of the pathogenesis of this disease. Aurora A and B kinases play different important roles in cell cycle control and genomic instability and have never been studied in endometriosis. The aim of this study was to compare the expression levels of Aurora kinases, Ki-67 and hormone receptor in endometriotic tissue (ET) and normal endometrium.
We retrospectively analysed 438 samples obtained from 194 patients affected by endometriosis and 28 samples from 28 patients with normal endometrium, which were all collected by the Pathology Department and Gynecologic Clinic of the University Hospital of Udine. A tissue microarray model was constructed to use immunohistochemistry to analyse the expression of Aurora A and B kinases, Ki-67 and the estrogen and progesterone receptors in ET and normal endometrium.
Aurora A and B kinases were expressed at a very low level in the majority of endometriosis core biopsies. Aurora A and B kinases, Ki-67 and the estrogen and progesterone receptors were expressed at a higher level in the proliferative endometrium than in the secretory endometrium and in ovarian and non-ovarian ET (P < 0.05). Additionally, Aurora B kinase, Ki-67 and the estrogen and progesterone receptors were more highly expressed in non-ovarian than ovarian ET (P < 0.05).
Considering the low expression levels of Aurora A and B kinases in the majority of endometriosis core biopsies, the growth and survival of endometrial tissue outside the uterus cannot be explained by deregulation of this pathway. The analysed ectopic endometrium protein expression pattern resembled that of the secretory endometrium, and markers of proliferation and hormone receptors were expressed at lower levels in ovarian than in non-ovarian ET. The low level of hormone receptors and the consequent low levels of proliferation markers in ovarian ETs may be due to down-regulation by the ovary's hormone milieu.
细胞增殖和基因组不稳定性在子宫内膜异位症中的作用是该疾病发病机制中备受争议的方面。Aurora A 和 B 激酶在细胞周期控制和基因组不稳定性中发挥着不同的重要作用，而在子宫内膜异位症中从未进行过研究。本研究旨在比较子宫内膜异位症组织（ET）和正常子宫内膜中 Aurora 激酶、Ki-67 和激素受体的表达水平。
我们回顾性分析了来自 194 名子宫内膜异位症患者的 438 个样本和 28 名正常子宫内膜患者的 28 个样本，这些样本均由乌迪内大学医院的病理科和妇科诊所收集。构建组织微阵列模型，使用免疫组织化学分析 Aurora A 和 B 激酶、Ki-67 以及雌激素和孕激素受体在 ET 和正常子宫内膜中的表达。
在大多数子宫内膜异位症核心活检中，Aurora A 和 B 激酶的表达水平非常低。Aurora A 和 B 激酶、Ki-67 以及雌激素和孕激素受体在增殖期子宫内膜中的表达水平高于分泌期子宫内膜和卵巢及非卵巢 ET（P<0.05）。此外，非卵巢 ET 中 Aurora B 激酶、Ki-67 以及雌激素和孕激素受体的表达水平高于卵巢 ET（P<0.05）。
考虑到大多数子宫内膜异位症核心活检中 Aurora A 和 B 激酶的低表达水平，不能用该途径的失调来解释子宫外子宫内膜的生长和存活。分析的异位子宫内膜蛋白表达模式类似于分泌期子宫内膜，并且在卵巢 ET 中增殖标志物和激素受体的表达水平低于非卵巢 ET。卵巢 ET 中激素受体水平低和随之而来的增殖标志物水平低可能是由于卵巢激素环境的下调所致。
