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Low expression of glucocorticoid receptor α in oral lichen planus correlates with activation of nuclear factor κ B : a preliminary study
Author(s) -
Lin Xuecai,
Sun Hongying,
Zhen Yuexiang,
Zhang Hui,
Shi Hang,
Wang Xiaxia
Publication year - 2014
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12168
Subject(s) - oral lichen planus , immunohistochemistry , glucocorticoid receptor , glucocorticoid , basal (medicine) , pathogenesis , stratum spinosum , medicine , chemistry , biology , pathology , endocrinology , insulin , stratum corneum
Background Emerging evidence indicates that the interaction between glucocorticoid receptor α ( GR α) and nuclear factor κB ( NF ‐κB) is a key pathogenetic cross talk in the autoimmune and inflammatory disorders. The objective of this study was to determine the GR α expression in patients with oral lichen planus ( OLP ) and investigate its correlation with NF ‐κB in OLP . Methods We compared the expression of GR α and NF ‐κB in oral biopsy specimens from patients with OLP ( n = 32) against normal controls ( n = 12) and investigated the correlation between the expression of GR α and NF ‐κB in OLP . Results Immunohistochemistry showed that GRα mainly expressed in the cytoplasm of keratinocytes of basal and spinosum layer of OLP . Both real‐time quantitative PCR and Western blots revealed that the mRNA and protein expression levels of GRα were decreased compared with normal controls (both P < 0.001). Conversely, those levels of nuclear factor‐kappa B (NF‐κB) were increased compared with normal controls (both P < 0.001). Importantly, a significant inverse correlation between the GRα and NF‐κB was found ( P < 0.05). Conclusions Our findings demonstrated that low expression of GR α in OLP correlates with activation of NF ‐κB, which indicates that the cross talk between GR α and NF ‐κB in OLP may become a new therapeutic target and represent a new approach to explore the pathogenesis of OLP .