Galectin-3 plays an important role in endometriosis development and is a target to endometriosis treatment

• Published in: Molecular and cellular endocrinology 2019-04, Vol.486, p.1-10
• Main Authors: Mattos, Rômulo Medina de, Machado, Daniel Escorsim, Perini, Jamila Alessandra, Alessandra-Perini, Jéssica, Meireles da Costa, Nathália de Oliveira, Wiecikowski, Adalgisa Felippe da Rocha de Oliveira, Cabral, Katia Maria dos Santos, Takiya, Christina Maeda, Carvalho, Renato Sampaio, Nasciutti, Luiz Eurico
• Format: Article
• Language: English
• Subjects: Angiogenesis; Animals; Biomarkers - metabolism; Endometriosis; Endometriosis - drug therapy; Endometriosis - metabolism; Endometrium - drug effects; Endometrium - pathology; Female; Gal3C; Galectin 3 - chemistry; Galectin 3 - metabolism; Galectin-3; Inflammation - pathology; Macrophages - drug effects; Macrophages - metabolism; Mice, Inbred BALB C; Mice, Knockout; Molecular Targeted Therapy; Neovascularization, Pathologic - drug therapy; Protein Domains; Recombinant Proteins - chemistry; Recombinant Proteins - pharmacology; Recombinant Proteins - therapeutic use; Therapeutic target; Vascular Endothelial Growth Factor A - metabolism; Vascular Endothelial Growth Factor Receptor-2 - metabolism
• ISSN: 0303-7207; 1872-8057
• DOI: 10.1016/j.mce.2019.02.007

This study aimed to analyze galectin-3 importance in endometriotic lesions development and the effect of recombinant Gal-3 carbohydrate recognition domain (Gal3C) in experimental endometriosis treatment. Experimental endometriosis was induced in WT and Gal-3−/− mice. Initially developed lesions were macroscopically and histologically analyzed, including immunohistochemical analysis. Then, WT mice were treated with Gal3C for 15 days. Gal-3 deficiency and Gal3C treatment significantly impaired endometriosis development. A significant decrease in lesions implantation and size, VEGF and VEGFR-2 expression, vascular density and macrophage distribution were observed in Gal-3 absence or inhibition. A greater presence of iNOS positive cells was observed in knockout mice lesions, while the presence of Arginase positive cells was higher in the WT animal lesions. In addition, COX-2 and TGFb1 were reduced by Gal3C treatment. Data showed here indicate a relevant role of Gal-3 in endometriosis development and highlight a target of endometriosis treatment using Gal-3 inhibitor. •Gal-3 absence or inhibition leads to impaired endometriotic lesions development.•Angiogenic markers and vascular density are decreased in Gal-3 absence/inhibition.•Macrophage population is reduced in Knockout or Gal3C treated endometriotic lesions.•Macrophage are majority iNOS positive in Gal-3 absence.