Programa de Pesquisa em Biologia Celular e do Desenvolvimento, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Cidade Universitária-Ilha do Fundão, 21941-590 Rio de Janeiro, RJ Brazil.
J Exp Clin Cancer Res. 2010 Jan 19;29(1):4. doi: 10.1186/1756-9966-29-4.
Endometriosis is a common disease characterized by the presence of a functional endometrium outside the uterine cavity, causing pelvic pain, dysmenorrheal, and infertility. This disease has been associated to development of different types of malignancies; therefore new blood vessels are essential for the survival of the endometrial implant. Our previous observations on humans showed that angiogenesis is predominantly found in rectosigmoid endometriosis, a deeply infiltrating disease. In this study, we have established the experimental model of rat peritoneal endometriosis to evaluate the process of angiogenesis and to compare with eutopic endometrium.
We have investigated the morphological characteristics of these lesions and the vascular density, VEGF and its receptor Flk-1 and MMP-9 expression, and activated macrophage distribution, using immunohistochemistry and RT-PCR.
As expected, the auto-transplantation of endometrium pieces into the peritoneal cavity is a well-established method for endometriosis induction in rats. The lesions were cystic and vascularized, and demonstrated histological hallmarks of human pathology, such as endometrial glands and stroma. The vascular density and the presence of VEGF and Flk-1 and MMP-9 were significantly higher in endometriotic lesions than in eutopic endometrium, and confirmed the angiogenic potential of these lesions. We also observed an increase in the number of activated macrophages (ED-1 positive cells) in the endometriotic lesions, showing a positive correlation with VEGF.
The present endometriosis model would be useful for investigation of the mechanisms of angiogenesis process involved in the peritoneal attachment of endometrial cells, as well as of the effects of therapeutic drugs, particularly with antiangiogenic activity.
子宫内膜异位症是一种常见疾病，其特征是子宫腔外存在功能性子宫内膜，导致盆腔疼痛、痛经和不孕。该疾病与不同类型的恶性肿瘤的发展有关；因此，新血管对于子宫内膜植入物的存活至关重要。我们之前对人类的观察表明，血管生成主要发生在直肠乙状结肠子宫内膜异位症中，这是一种深度浸润性疾病。在这项研究中，我们建立了大鼠腹膜子宫内膜异位症的实验模型，以评估血管生成过程，并与在位子宫内膜进行比较。
我们通过免疫组织化学和 RT-PCR 研究了这些病变的形态特征以及血管密度、VEGF 及其受体 Flk-1 和 MMP-9 的表达和激活的巨噬细胞分布。
正如预期的那样，将子宫内膜片自体移植到腹腔中是诱导大鼠子宫内膜异位症的一种成熟方法。病变呈囊性和血管化，具有人类病理学的组织学特征，如子宫内膜腺体和基质。与在位子宫内膜相比，子宫内膜异位症病变中的血管密度以及 VEGF、Flk-1 和 MMP-9 的存在显著增加，证实了这些病变的血管生成潜力。我们还观察到子宫内膜异位症病变中激活的巨噬细胞（ED-1 阳性细胞）数量增加，与 VEGF 呈正相关。
本子宫内膜异位症模型将有助于研究子宫内膜细胞腹膜附着过程中的血管生成机制，以及治疗药物的作用，特别是具有抗血管生成活性的药物。
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