Purpose: Despite recent advances in the diagnosis and treatment of
rheumatoid arthritis (RA), this inflammatory disease remains a challenge to patients and physicians. Recent evidence highlights the contribution of endoplasmic reticulum (ER) stress in the pathogenesis and treatment of RA. Herein, we study the expression of the ER stress sensor
inositol-requiring
enzyme 1α (IRE1α), as well as XBP1 splicing and the regulated IRE1-dependent decay (RIDD), in peripheral blood mononuclear cells (PBMCs) from patients with RA compared with healthy controls. Methods: The PBMCs from blood samples of RA patients and healthy volunteers were isolated by a density gradient centrifugation method using
Ficoll. The gene expression levels of
GRP78/ Bip, IRE1, XBP1s, micro-RNAs (
miRNAs) were evaluated by real-time PCR. Results: The expression of
GRP78, IRE1, and XBP1s were increased in PBMCs of RA patients compared with healthy controls. We further show that the RIDD targets (miRNA-17, -34a, -96, and -125b) were downregulated in RA samples. Conclusion: This study can expand our knowledge on the importance of
RNase activity of IRE1α in RA and may offer new potentials for developing novel diagnostic and/or therapeutic
biomarkers.