Da Costa Katiane de Almeida, Malvezzi Helena, Dobo Cristine, Neme Rosa Maria, Filippi Renée Zon, Aloia Thiago Pinheiro Arrais, Prado Elisa Rampazo, Meola Juliana, Piccinato Carla de Azevedo
Hospital Israelita Albert Einstein, São Paulo, Brazil.
Department of Clinical Pathology, Hospital Israelita Albert Einstein, São Paulo, Brazil.
Front Mol Biosci. 2022 May 3;9:854991. doi: 10.3389/fmolb.2022.854991. eCollection 2022.
Endometriosis is a highly prevalent gynecological disease characterized by lesions in different sites. Regulation of specific estrogen pathways may favor the formation of distinct microenvironments and the progression of endometriosis. However, no study has simultaneously evaluated the gene and protein regulation of the main estrogen-synthesizing enzymes in endometriosis. Thus, our goals were to study the relationship between gene and protein expression of aromatase ( or ARO), steroid sulfatase (STS), and hydroxysteroid 17-beta dehydrogenase (HSD17B1) in superficial (SUP), ovarian (OMA), and deep infiltrating (DIE) endometriotic lesion sites as well as in the eutopic endometrium of patients with (EE) and without (control) endometriosis in the same and large cohort of patients. The site-specific expression of these enzymes within different cells (glandular and stromal components) was also explored. The study included 108 patients surgically diagnosed with endometriosis who provided biopsies of EE and endometriotic lesions and 16 disease-free patients who collected normal endometrium tissue. Our results showed that was detected in all endometriosis tissues and was in higher levels than in control. Unique patterns of the and levels showed that they were most closely regulated in all tissues, with manifestation at greater levels in DIE compared to the other endometriotic lesion sites, OMA and SUP. Gene and protein expression of ARO, STS, and HSD17B1 occurred at different rates in endometriotic sites or EE. The distinctive levels of these estrogen-synthesizing enzymes in each endometriotic site support the hypothesis of a tissue microenvironment that can both influence and be influenced by the expression of different estrogenic pathways, locally affecting the availability of estrogen needed for maintenance and progression of endometriotic lesions.
子宫内膜异位症是一种高度常见的妇科疾病，其特征是在不同部位出现病变。特定雌激素途径的调节可能有利于不同微环境的形成以及子宫内膜异位症的进展。然而，尚无研究同时评估子宫内膜异位症中主要雌激素合成酶的基因和蛋白质调节情况。因此，我们的目标是研究芳香化酶（或ARO）、类固醇硫酸酯酶（STS）和17-β-羟基类固醇脱氢酶（HSD17B1）在浅表性（SUP）、卵巢性（OMA）和深部浸润性（DIE）子宫内膜异位病变部位以及患有（EE）和未患（对照）子宫内膜异位症患者的在位内膜中的基因和蛋白质表达之间的关系，研究对象为同一大组患者。还探讨了这些酶在不同细胞（腺和基质成分）内的位点特异性表达。该研究纳入了108例经手术诊断为子宫内膜异位症的患者，他们提供了在位内膜和子宫内膜异位病变的活检样本，以及16例无病患者，他们采集了正常子宫内膜组织。我们的结果显示，在所有子宫内膜异位症组织中均检测到了[此处原文缺失相关物质]，且其水平高于对照组。[此处原文缺失相关物质]和[此处原文缺失相关物质]水平的独特模式表明，它们在所有组织中受到最密切的调节，与其他子宫内膜异位病变部位OMA和SUP相比，在DIE中的表现水平更高。ARO、STS和HSD17B1的基因和蛋白质表达在子宫内膜异位症部位或在位内膜中以不同速率发生。每个子宫内膜异位症部位中这些雌激素合成酶的独特水平支持了组织微环境假说，该微环境既能影响不同雌激素途径的表达，又会受到其影响，从而局部影响维持和进展子宫内膜异位病变所需雌激素的可用性。
