Department of Obstetrics and Gynecology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230036, China; Institute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Science and Medical Center, University of Science and Technology of China, Hefei, Anhui 230001, China.
Department of Obstetrics and Gynecology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230036, China; Institute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Science and Medical Center, University of Science and Technology of China, Hefei, Anhui 230001, China.
J Reprod Immunol. 2022 Jun;151:103513. doi: 10.1016/j.jri.2022.103513. Epub 2022 Mar 14.
Endometriosis is a common estrogen-dependent gynecological disorder that is characterized by endometrial-like tissue being found at extrauterine sites. Aberrant expression and activation of estrogen receptor beta (ERβ) in ectopic endometrium are involved in endometriosis development. Here, we used primary tissues and cells from endometriosis patients to investigate the molecular mechanisms involved in ERβ's contribution to endometriosis progression. Through RNA-seq, quantitative PCR, and immunohistochemistry analysis, we found that ERβ expression is related to the severity of endometriosis; specifically, the ratio of ESR2/ESR1 in ectopic tissues was positively correlated with the severity of endometriosis, which suggests that ERβ has a predominant role in endometriosis progression. Furthermore, we found that ERβ could bind to the CD47 promoter, increasing CD47 expression levels. CD47 is a critical molecule in "don't eat me" signaling. These data highlight the importance of the ERβ-CD47 axis in the pathogenesis of endometriosis. We believe targeting CD47 may be a novel therapeutic approach for treating endometriosis and other ERβ-associated diseases.
子宫内膜异位症是一种常见的雌激素依赖性妇科疾病，其特征是在子宫外部位发现类似子宫内膜的组织。异位子宫内膜中雌激素受体β（ERβ）的异常表达和激活参与了子宫内膜异位症的发展。在这里，我们使用子宫内膜异位症患者的原代组织和细胞，研究了 ERβ 促进子宫内膜异位症进展的分子机制。通过 RNA-seq、定量 PCR 和免疫组织化学分析，我们发现 ERβ 的表达与子宫内膜异位症的严重程度有关；具体来说，异位组织中 ESR2/ESR1 的比值与子宫内膜异位症的严重程度呈正相关，这表明 ERβ 在子宫内膜异位症的进展中起主要作用。此外，我们发现 ERβ 可以与 CD47 启动子结合，增加 CD47 的表达水平。CD47 是“不要吃我”信号中的关键分子。这些数据强调了 ERβ-CD47 轴在子宫内膜异位症发病机制中的重要性。我们相信靶向 CD47 可能是治疗子宫内膜异位症和其他 ERβ 相关疾病的一种新的治疗方法。
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