Expression of endoplasmic reticulum stress-related molecule in oral lichen planus

Abstract

Oral lichen planus (OLP) is known as a T cell-mediated autoimmune disease. Apoptosis and T cell recruitment are thought to play major roles in pathogenesis of OLP. The apoptosis is reported to be mediated by extrinsic, intrinsic, and perforin/granzyme B apoptotic pathway, but the exact mechanisms of apoptosis are unknown in OLP. Recently, an endogenous cellular stress, endoplasmic reticulum (ER) stress, emerges a new apoptotic signaling initiator and controls inflammation and immune response. ER stress is also thought to play an important role in development of T cell-mediated autoimmune diseases. Further, it has been reported that ER stress regulates an endogenous inhibitor of leukocyte adhesion that is critical in leukocyte recruitment. The aim of this study is to investigate a potential role of ER stress in pathogenesis of OLP. We examined the expression of B cell immunoglobulin protein (BIP); an ER stress marker, tumor necrosis factor alpha (TNF-α); a potent modulator of cellular apoptosis, CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP); a transcription factor involved in ER stress-induced apoptosis, and developmental endothelial locus-1 (Del-1); an endogenous inhibitor of leukocyte adhesion by reverse transcription-polymerase chain reaction and immunohistochemistry in OLP tissue. The mRNA expression level of BIP and TNF-α were significantly higher, and CHOP was significantly lower in OLP compared to the control. The mRNA expression level of Del-1 was not significantly different between the control and OLP. CHOP was expressed in the upper epithelial layers in the control, whereas, expressed in the basal epithelial layer in OLP. Del-1 was not expressed in the endothelial cell of the control, but expressed in the endothelial cells of OLP. We found out that ER stress is increased in OLP lesion and ER stress-induced apoptosis may be involved in apoptosis of basal keratinocytes. We suggest that the endogenous cellular stress, ER stress, may play a role in pathogenesis of OLP and propose that ER stress could be a new scope for study of OLP.