Expression of receptors for TGF-B Superfamily in cows with spontaneous and ACTH-induced cystic ovarian disease

MATILLER V; HEIN G; AMWEG AN; RODRIGUEZ FM; BERTOLI J; QUERCIA E; REY F; SALVETTI NR

Mar del Plata

Congreso; LXI Reunión Científica Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2016

SAIC

Preliminary results showsignificant changes in the expression of components of the TGF-B isoformsTGF-B1, 2 and 3, and inhibin / activin / follistatin system in ovarianstructures of dairy cattle with spontaneous and ACTH-induced cystic ovariandisease (COD). Given the evidence of its role as an important molecules in paracrineand autocrine signalling pathways that regulate the growth of ovarian follicle,and knowing that this components carry out their actions through binding to twotypes of membrane receptors, the objective of the present work was examine theexpression of TGF-B receptor (TGF-BR)I, TGF-BRII, TGF-BRIII, Activin Receptor(ACVR)IB and ACVRIIB in ovaries of cows with COD previously evaluated for theirrelated ligands. We worked withsections obtained from bovine ovaries with spontaneous COD (n=10), ACTH-inducedCOD (n=10), and controls ovaries (n=10). In 4 um thick sections, the presence andexpression of receptors was determined by indirect immunohistochemistry ingranulosa and theca cells. Type I receptors expressed higher staining (p<0.05) in tertiary follicles of spontaneous COD group than controlsfollicles, and type II receptor ACVRIIB, showed higher immunostaining in thecacells of spontaneous COD group than control. Here we detected changes in the expressionof the receptors necessary for the response to the growth factors of TGF-Bfamily in the COD cow?s ovaries in relation to the controls. The highexpression of all receptors analyzed in follicular cysts could be linked to the persistence over time of these structures. We can conclude that alterations found at ligands level materialize achange in signalling favouring these actions at the cellular level. Thus, tounravel intraovarian signalling pathways, we postulate data that may contributeto the knowledge of the pathogenesis of COD and that can be applicable to thedesign of protocols and therapeutic measures.