CONICET | Buscador de Institutos y Recursos Humanos

Endometriosis is characterized by the presence of endometrial tissue outside the uterine cavity and is well known that vascular development is essential for ectopic lesion growth. Galectin-1 (Gal-1) is an endogenous lectin that binds to N-acetyllactosamine disposed on cell surface glycoproteins, and plays an essential role as immunomodulatory and pro-angiogenic factor in tumor development. Until now, it has not been reported the involvement of Gal-1 in endometriosis pathophysiology. Thus, our main goal was to study the role of Gal-1 in growth and vascular development of ectopic lesions. Methods: Endometriotic-like lesions were experimentally induced in female C57BL/6 wild-type mice and knockout for Gal-1 (Lgals1-/ -) by autologous or heterologous transplantation of endometrial tissue to bowel mesentery. In addition, one wild-type endometriosis group was intraperitoneally injected with a Gal-1 blocking antibody. After four weeks, the number, and volume of lesions were assessed. Also, the vascularized area and the number of blood vessels were measured by immunohistochemistry for the von Willebrand factor (vWF) and the vascular endothelial growth factor receptor-2 (VEGFR-2). Results: There was a significant reduction of lesion size in Lgals1-/ - and heterologous KO mice, as well as in mice treated with Gal-1 blocking antibody. Moreover, the vascular area and number of blood vessels immunostained for vWF was significantly lower in Lgals1-/-and heterologous KO mice lesions, but no changes were observed in the endothelial expression of VEGFR-2. Conclusion: These results strongly suggest that Gal-1 plays a pivotal role in the vascular development and consequently in the growth of endometriotic lesions.