Impact of the Reticular Stress and Unfolded Protein Response on the inflammatory response during the implantation period

ELIZABETH SOCZEWSKI, ESTEBAN GRASSO, LAURA FERNÁNDEZ, LUCILA GALLINO, CLAUDIA PÉREZ LEIRÓS AND ROSANNA RAMHORST

Mar del Plata

Congreso; Reunión anual conjunta de la Sociedad Argentina de Investigación Clínica y de la Sociedad Argentina de Inmunología; 2016

SAI-SAIC

Embryo implantation in humans involves the generation of an inflammatory response associated with invasion of the blastocyst in the decidua. This inflammatory response is sterile and could be induced by endogenous ligands released during tissue remodeling, however, it is still unclear whether other processes are involved. At decidualization, cells undergo reticular stress (RS) and unfolded protein response (UPR), which will allow them to expand their endoplasmic reticulum with the corresponding machinery for protein folding. Here, we focus on the impact of RS and UPR on endometrial and decidual cells and whether they induce a physiological sterile inflammatory response through IL-1beta. We used an in vitro model of human decidualization represented by Human endometrial stromal cell line (HESC) treated or not with VIP 10-7M (vasoactive intestinal peptide known to induce decidualization) or with medroxiprogesterone (MPA 10-6M) and dbcAMP (2,5 10-3M) during 8 days. First, we evaluated the RS by the expression of the 3 sensors, ATF6, PERK and IRE1. Decidualized cells in the presence of VIP or MPA increased the expression of ATF6 and PERK while did not modulate IRE1. This effect was also observed in the presence of Thapsigargin (Tg 2ug/ml) for both sensors (p