Abstract

We previously identified a novel apoptosis inducing humoral factor in the conditioned medium of hypoxic/ reoxygenated cardiac myocytes. Myocardial ischemia/reperfusion markedly increased plasma ORAIP levels and myocardial ischemia/reperfusion injury was clearly suppressed by neutralizing anti-ORAIP antibodies in vivo. We named this novel post-translationally modified secreted-form of eukaryotic translation initiation factor 5A, as Oxidative Stress-Responsive Apoptosis Inducing Protein (ORAIP). Evidence has accumulated that ORAIP may be a common and the dominant apoptosis-inducer among various cell types in response to various types of oxidative stress involved in a wide spectrum of acute and chronic disorders. We found infiltrating immune cells strongly expressed ORAIP in the tissues with myocarditis, aortitis, and atherosclerosis, suggesting that ORAIP-mediated apoptotic signalling may play a role in the pathogenesis involved. Further investigation is needed to confirm whether ORAIP can be a sensitive biomarker and a therapeutic target for the cell injury involved in immune disorders.

Keywords: Eukaryotic translation initiation factor 5A (eIF5A); Ischemia/reperfusion (I/R) injury; Oxidative stress; Oxidative Stress-Responsive Apoptosis Inducing Protein (ORAIP)