Abstract
To characterize the patterns of cell differentiation, proliferation, and tissue invasion in eutopic and ectopic endometrium of rabbits with induced endometriotic lesions via a well- known experimental model, 4 and 8 weeks after the endometrial implantation procedure. Twenty-nine female New Zealand rabbits underwent laparotomy for endometriosis induction through the resection of one uterine horn, isolation of the endometrium, and fixation of tissue segment to the pelvic peritoneum. Two groups of animals (one with 14 animals, and the other with15) were sacrificed 4 and 8 weeks after endometriosis induction. The lesion was excised along with the opposite uterine horn for endometrial gland and stroma determination. Immunohistochemical reactions were performed in eutopic and ectopic endometrial tissues for analysis of the following markers: metalloprotease (MMP-9) and tissue inhibitor of metalloprotease (TIMP-2), which are involved in the invasive capacity of the endometrial tissue; and metallothionein (MT) and p63, which are involved in cell differentiation and proliferation. The intensity of the immunostaining for MMP9, TIMP-2, MT, and p63 was higher in ectopic endometria than in eutopic endometria. However, when the ectopic lesions were compared at 4 and 8 weeks, no significant difference was observed, with the exception of the marker p63, which was more evident after 8 weeks of evolution of the ectopic endometrial tissue. Ectopic endometrial lesions seem to express greater power for cell differentiation and tissue invasion, compared with eutopic endometria, demonstrating a potentially invasive, progressive, and heterogeneous presentation of endometriosis.
Highlights
The etiopathogenesis of endometriosis is controversial.[1]
We have demonstrated that the ectopic endometrial lesions showed a higher number of immune stained cells expressing cellular invasion markers (MMP-9 and its inhibitor tecidual da metaloprotease 2 (TIMP-2)) and of molecules involved in cellular proliferation and differentiation (MT and p63) than the eutopic endometrial lesions, using a rabbit experimental model of endometriosis
The progression time of these lesions did not interfere in a statistically significant way in the MMP-9 (p 1⁄4 0.214) and in the tissue inhibitors of MMPs (TIMPs)-2 staining (p 1⁄4 0.66), our results suggest that the evaluation of MMP-9 and TIMP-2 could be used as a prognostic indicator of endometrial invasion; increasing the proteolytic activity would be one of the many factors that contribute to the invasive properties of the endometrium, resulting in the development of endometriosis
Summary
The etiopathogenesis of endometriosis is controversial.[1]. Several theories have been proposed, such as the presence of retrograde menstrual flow associated with an immunological predisposition in the peritoneal microenvironment that facilitates the implantation of viable endometrial cells and has the potential for implantation.[2]. Metalloproteases are a family of endopeptidases that play a role in degrading and remodeling the extracellular matrix They are zinc dependent and include collagenase, gelatinase, and stromal enzymes. Their activities are regulated by TIMPs.[20] The production of MMPs and of TIMPs occurs in the endometrial stroma and in the epithelium, as well as in polymorphonuclear leucocytes. Another important source of these enzymes are macrophages, neutrophils, and eosinophils, activated in response to a certain degree of inflammation present in the peritoneal cavity of women with endometriosis.[21,22,23]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Revista Brasileira de Ginecologia e Obstetrícia / RBGO Gynecology and Obstetrics
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
