Bacallao K, Plaza-Parrochia F, Cerda A, Gabler F, Romero C, Vantman D, Vega M
Department of Obstetrics and Gynecology, School of Medicine, University of Chile Clinical Hospital, Santiago, Chile Interdisciplinary Stem Cell Institute, University of Miami, Miller School of Medicine, Miami, FL, USA.
Department of Obstetrics and Gynecology, School of Medicine, University of Chile Clinical Hospital, Santiago, Chile.
Reprod Sci. 2016 Feb;23(2):211-8. doi: 10.1177/1933719115597762. Epub 2015 Aug 2.
Polycystic ovarian syndrome (PCOS) has been associated with endometrial hyperplasia and cancer. The aim of this study was to establish whether the expression of proliferation regulatory proteins in the endometria of patients having PCOS, with or without hyperplasia, differs from control women. Control endometria (CE), patients having PCOS without and with endometrial hyperplasia (PCOSE and HPCOSE, respectively), and that of women with endometrial hyperplasia (HE) were used. The phosphorylated estrogen receptor form (pERα), similar to mother against decapentaplegic (SMAD) 2, SMAD3, and SMAD4, vascular epithelial growth factor (VEGF), and phosphorylated SMAD (pSMAD) 2 and pSMAD3 were detected by immunohistochemistry or Western blot. The results show higher levels of pERα in HE versus CE (P < .05), while higher VEGF levels were found in PCOSE and HE (P < .05) compared to CE; SMAD2 diminished in HE (P < .05) versus CE. Consequently, the higher levels of VEGF and pERα in PCOSE could represent early changes in the progression of PCOSE toward hyperplasia and cancer, whereas changes observed in SMAD proteins support the differential origin of the pathologies of HPCOSE and HE.
多囊卵巢综合征（PCOS）与子宫内膜增生和癌症有关。本研究的目的是确定患有PCOS（无论有无增生）的患者子宫内膜中增殖调节蛋白的表达是否与对照女性不同。使用对照子宫内膜（CE）、无子宫内膜增生和有子宫内膜增生的PCOS患者（分别为PCOSE和HPCOSE）以及子宫内膜增生女性（HE）的子宫内膜。通过免疫组织化学或蛋白质印迹法检测磷酸化雌激素受体形式（pERα）、与果蝇的母亲抗五体不全蛋白（SMAD）2、SMAD3和SMAD4、血管内皮生长因子（VEGF）以及磷酸化SMAD（pSMAD）2和pSMAD3。结果显示，与CE相比，HE中的pERα水平更高（P <.05），而与CE相比，PCOSE和HE中的VEGF水平更高（P <.05）；与CE相比，HE中的SMAD2减少（P <.05）。因此，PCOSE中较高水平的VEGF和pERα可能代表PCOSE向增生和癌症进展的早期变化，而SMAD蛋白的变化支持HPCOSE和HE病理的不同起源。
