Targeting the galectin-1-mediated angiogenesis at peritoneal level is crucial to constrain the progress of endometriosis.

BASTÓN JI; BARAÑAO RI; BILOTAS M; CROCI D; RAVINOVICH G; MERESMAN GF

Congreso; 12th World congress on endometriosis.; 2014

Objective: The endogenous lectin, Galectin-1 (Gal-1), plays a pivotal role in the vascular development and consequently growth of endometriotic lesions. A targeted blockade of Gal-1 at peritoneal level was performed with the aim to evaluate an experimental approach that could shed light on a future potential therapeutic strategy for the endometriosis. Design: Endometriosis was surgically induced in C57BL/6 mice. Targeted blockade of Gal-1 at peritoneal level was carried out with a neutralizing anti-galectin-1 monoclonal antibody. The number and size of developed endometriotic lesions, besides the relative vascularized area and the peritoneal content of proangiogenic cytokines were assessed. Material and methods: Endometriotic-like lesions were induced in C57BL/6 by autologous transplantation of endometrial tissue to bowel mesentery. Six mice were injected intraperitoneally 3 times for week with 15 mg/kg of the neutralizing anti-Gal-1 antibody F8.G7, and 6 mice with the IgG isotype antibody, from second to fourth week post endometriosis induction. Results: Despite there was no change in the number of developed endometriotic lesions between groups, notably, the peritoneal blockade of Gal-1 resulted in a significant reduction of lesions size in anti-Gal-1 treated mice compared to controls (P