In a study published January 19, 2010, researchers let us know that previous studies show for a fact that angiogenesis is largely found in rectosigmoid endometriosis (found near the sigmoid colon and the upper part of the rectum), and it embeds deeply.
In this new study, researchers experimental with peritoneal endometriosis (endo found in the thin transparent membrane that lines the abdominal cavity) in rats to watch the process of angiogenesis, and to compare what they saw with normal endometrium.
They concluded that rogue cell growth of endo does of course proliferate in the peritoneum, and would like to use this study to open the door to develop antiangiogenic drugs to prevent such rogue cell growth – to help prevent the spread of endometriosis.
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.
Methods: 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.
Results: 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.
Conclusion: 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.
Author: Daniel MachadoPlinio BerardoCelia PalmeroLuiz Nasciutti
Credits/Source: Journal of Experimental &Clinical Cancer Research 2010, 29:4
Published on: 2010-01-19
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