Targeting the galectin-1-mediated angiogenesis at peritoneal level constrains the progress of endometriosis'

BASTÓN JI; BARAÑAO RI; BILOTAS M; CROCI D; RABINOVICH GA; MERESMAN G.

Sao Paulo

Congreso; 12th World Congress on Endometriosis,; 2014

World Endometriosis Society

Objectives: 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 endometriosis. Design: Endometriosis was surgically induced in C57BL/6 mice by autologous transplantation of endometrial tissue to bowel mesentery. Mice were injected intraperitoneally from post-surgical day 14 and continued until day 28, 3 times a week with 15 mg/kg of the neutralizing anti-Gal-1 antibody F8.G7 (Anti-Gal-1), or with the IgG isotype antibody (Control). Materials and Methods: The number and size of endometriotic lesions were evaluated in Anti-Gal-1 and Control groups at the post-surgical day 28. The relative vascularized area was assessed by immunohistochemistry in lesions and the concentrations of proangiogenic factors were measured in peritoneal fluid by ELISA, in both groups. Results: Despite there was no significant difference 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