| Literature DB >> 30753853 |
Rômulo Medina de Mattos1, Daniel Escorsim Machado2, Jamila Alessandra Perini3, Jéssica Alessandra-Perini2, Nathália de Oliveira Meireles da Costa4, Adalgisa Felippe da Rocha de Oliveira Wiecikowski5, Katia Maria Dos Santos Cabral6, Christina Maeda Takiya7, Renato Sampaio Carvalho5, Luiz Eurico Nasciutti8.
Abstract
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.Entities:
Keywords: Angiogenesis; Endometriosis; Gal3C; Galectin-3; Therapeutic target
Mesh：
Substances：
Year: 2019 PMID： 30753853 DOI： 10.1016/j.mce.2019.02.007
Source DB: PubMed Journal: Mol Cell Endocrinol ISSN： 0303-7207 Impact factor: 4.102