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Ca2+‐Induced Mitochondrial Oxidative Stress Mediates Disruption of Intestinal Epithelial Tight Junction: Activation of a Similar Signaling Cascade in Colon by Chronic Restraint Stress

Intestinal epithelial tight junctions (TJ) plays a crucial role in establishing the mucosal barrier function, by which it prevents diffusion of toxins, allergens and pathogens into intestinal tissue and systemic circulation. Our previous studies showed that osmotic stress (OS), dextran sulfate sodium (DSS) and cyclic stretch disrupt intestinal epithelial TJ and induce barrier dysfunction by a common mechanism involving Ca2+ channels, Ca2+ influx and Ask1/MAPKK/JNK/c‐Src signaling cascade. Oxidative stress is well known to disrupt intestinal epithelial TJ. IN the present study we investigated the role of mitochondrial oxidative stress in OS and DSS‐induced TJ disruption in Caco‐2 cell monolayers in vitro and activation of a similar signaling cascade in mouse colon by chronic restraint stress (CRS) in vivo.