IRE1α Promotes Cell Apoptosis and an Inflammatory Response in Endoplasmic Reticulum Stress-Induced Rheumatoid Arthritis Fibroblast-Like Synovial Cells by Enhancing Autophagy

Endoplasmic reticulum (ER) stress can induce autophagy via the unfolded protein response (UPR), and regulate activation of inflammasomes. Inositol-requiring enzyme 1α (IRE1α) is a transducer UPR in cells with ER stress. Here, we investigated role IRE1α its impact on rheumatoid arthritis fibroblast-like synovial (RA-FLSs). RA-FLSs were isolated from (RA) patients stimulated thapsigargin (TG) to produce cells. stress-, expression apoptosis-associated factors by western blotting qRT-PCR. Cellular ROS levels assessed flow cytometry. ELISAs performed determine concentrations inflammatory mediators. TG treatment promoted IRE1α, GRP78, CHOP, ATP6 mRNA expression. generation was increased TG-induced RA-FLSs; additionally, found cell inflammation upregulating inflammasome markers The markers, proteins, TG-stimulated RA-FLSs. However, transfection si-IRE1α suppressed increases generation, levels, apoptosis, Treatment activator RAPA attenuated protective effects silencing RA-FLS apoptosis damage. Our findings showed that RA-FLSs, alleviated stress-induced caused autophagy.