ENDOPLASMIC RETICULUM STRESS THROUGH ATF6A PATHWAY INDUCES AN INFLAMMATORY RESPONSE: POTENTIAL REGULATION BY MIRNAS

SOCZEWSKI E; MURRIETA-COXCA JM; MIRANDA L; GUTIÉRREZ SAMUDIO R; GALLINO L; GRASSO E; FERNÁNDEZ L; GORI S; MARTÍ M; MORALES-PRIETO D; FAVARO R; PÉREZ LEIRÓS C; MARKERT U; RAMHORST R

Congreso; Reunión Anual de Sociedades de Biociencias; 2020

During decidualization, endometrial stromal cells undergo endoplasmic reticulum stress (ERS) and unfolded protein response (UPR), which will allow them to expand their endoplasmic reticulum with the corresponding machinery for protein folding. These processes are directed by miRNAs that regulate the expression or stability of their transcription factors. Here we focus on the role of ERS/UPR during decidualization to induce a physiological sterile inflammatory response and whether it might be regulate by miRNAs. We used anin vitro model of decidualization represented by human telomerase-immortalized endometrial stromal cell line St-T1b, treated with 8-Br-cAMP (0.5 mM) during 5 days, or Thapsigargin (Tg, a RS-inducer 1 µg/ml); and endometrial biopsies from patients with recurrent spontaneous abortions (RSA) and recurrent in vitrofertilization failures (RIF). We evaluated the expression of the ERS-sensor ATF6 and the UPR marker, CHOP. Both markers increased in decidualized cells, and Tg induced even higher levels in comparison with non-decidualized cells (p