Subunidade alfa da inibina e seu correceptor betaglicano na endometriose

• Ano de defesa: 2010
• Autor(a) principal: Quesia Tamara Mirante Ferreira
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Endometriose; Endométrio; Imuno-histoquímica; Betatglicano; -inibina; Inibinas; Endometriose/etiologia; Expressão gênica
• Link de acesso: http://hdl.handle.net/1843/BUOS-8ZFNXJ

Endometriosis is a complex gynecologic disease associated with pelvic pain and infertility. It´s characterized by the presence of ectopic endometrial tissue and its pathogenesis remains to be fully described. Inhibins and activins are glycoproteins that belong to the transforming growth factor- (TGF-) superfamily, and betaglycan is an inhibin coreceptor. These molecules were identified as potential modulators of many biologic processes including cell proliferation, differentiation, and cellular fate determination. Also, previous studies have linked these glycoproteins and proteoglycan to the endometriosis pathogenesis. The aim of the present study was to evaluate the mRNA levels and protein distribution of the -inhibin subunit and betaglycan in endometriotic lesions and eutopic endometrium from women with or without endometriosis. Alfa-inhibin subunit and betaglycan gene expression were evaluated by quantitative real time PCR, and tissue protein distribution was assessed by immunohistochemistry. Alfa-inhibin and betaglycan mRNA's were expressed by eutopic endometrium from women with or without endometriosis but it was significantly higher in the endometrium of women with endometriosis. Immunostaining for -inhibin and betaglycan was found in both endometrial compartments: glands and stroma, and also in eutopic and ectopic endometrium. In patients with endometriosis, the -inhibin and betaglycan tissue distribution were less abundant in ectopic lesions than in eutopic endometrium. In conclusion, our results showed gene and protein expression of -inhibin and betaglycan in eutopic and ectopic endometrium. These findings suggest that these molecules could play a role in the pathogenesis of endometriosis.