GALECTIN-1 ROLE IN ENDOMETRIOSIS PATHOPHYSIOLOGY

BASTÓN, JUAN IGNACIO; RICCI, ANALÍA GABRIELA; BILOTAS, MARIELA ANDREA; OLIVARES, CARLA NOEMÍ; RABINOVICH, GABRIEL; BARAÑAO, ROSA INÉS; MERESMAN, GABRIELA FABIANA

Congreso; XII Jornadas Multidisciplinarias de la Sociedad Argentina de Biología (SAB); 2010

Endometriosis (EDT) is characterized by the ectopically occurrence of endometrial tissue reassembled in peritoneal or ovarian lesions. EDT is a common benign illness that affects 10% of women in reproductive age and its pathogenesis still remains unknown. Galectin-1 belongs to a family of endogenous lectins and has binding-affinity for multiple N-acetyllactosamine residues comprised on N- and O- glycans. This lectin is a key immunoregulatory, pro-angiogenic and growth-promoting factor in tumors. Data have not been reported on the role of Gal-1 in EDT etiology yet. Our hypothesis is that Gal-1 expression in endometriotic lesions improves endometrial cell survival and growth at the ectopic sites. In this study, we induced endometriotic lesions in female C57BL/6 wild-type and Gal-1 knock-out (Lgals1-/-) mice. Four weeks later the number and size of lesions was recorded and the cell proliferation and % vascularized area in the lesions were evaluated by immunohystochemistry for PCNA and CD34 markers respectively. Results show a significant decrease of lesion size (p<0.05), proliferating cell-rate (p<0.05) and vascularized area (p<0.01) in Gal-1 null mice. These results suggest that Gal-1 favours EDT development promoting ectopic endometrial cell proliferation and lesion vasculature expansion.