These results were in agreement TPCA-1 with those of Dogan et al. (2004) [25], who reported that the endometrial explants produced viable implants in 26 of 30 animals (86.6%), and that most of the explants were well vascularized. Analyses of the assessed microvessel density demonstrated that angiogenesis is higher in endometriotic lesions compared with the eutopic endometrium. Microvessel density was determined on the basis of vWF and α-SMA-positive vessels. The distribution of these vessel markers was more positive in stroma around the glands

in samples of endometriosis. Although no significant difference was observed between the vWF positive vessels in the two groups, the immunoreaction seemed to be more intense on day 15. It could be related to the microvessel size and that the endothelial Small molecule library chemical structure cell might not be adjacent to other pericyte

or vice versa. By other hand, the α-SMA-positive vessels were more numerous in samples of endometriosis at day 30 than at day 15. This difference is related to the fact that the most of the blood vessels are mature, as illustrated by their association with αSMA-positive pericytes [4]. These observations indicated that the development of new vessels is necessary for the establishment and the maintenance of the endometriotic lesions, and also that the selleck products neovessels formed were more mature in endometriosis after 30 days. Using the same markers in the nude-mouse model of endometriosis, Nap et al. (2004) [19] demonstrated that the development of new blood vessels remains of pivotal importance for the maintenance and growth

of endometriosis. One of the main characteristics of endometriosis is its inflammatory nature. It has been shown that cytokines released from immune cells play an important role in the pathogenesis of endometriosis, and many of these cytokines possess angiogenic activity [26, 27]. VEGF is the most-prominent and most-studied proangiogenic factor in endometriosis, and it is widely believed that VEGF is the main stimulus for angiogenesis and increased vessel permeability GNA12 in this disease [6]. Its activity depends on its binding to different receptors, such as VEGFR-2 (Flk-1). In our model, we were able to demonstrate that the expression of VEGF and Flk-1 is enhanced in endometriotic lesions as compared with controls. Their immunodistributions were observed focally in the cytoplasm of endothelial and glandular epithelial cells and diffusely in stromal cells, and were more intense in ectopic endometrial tissues. It was also observed that the number of activated macrophages (ED-1 positive cells) increased in endometriotic lesions. These results are in agreement with other studies that have shown that VEGF is strongly expressed by endometriotic lesions and activated macrophages [12, 28].