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Altered expression of CCN1 in oral lichen planus associated with keratinocyte activation and IL‐1β, ICAM1, and CCL5 up‐regulation
Author(s) -
Wang Yun,
Du Guanhuan,
Shi Linjun,
Shen Xuemin,
Shen Zhengyu,
Liu Wei
Publication year - 2020
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.13087
Subject(s) - ccl5 , keratinocyte , oral lichen planus , biology , microbiology and biotechnology , cancer research , immunology , cell culture , genetics , t cell , immune system , il 2 receptor
Background Emerging evidence indicates that CCN1 is a novel inflammation‐regulated mediator involved in the pathogenesis of some immune‐mediated inflammatory diseases. The objective of this study was to investigate the preliminary roles of CCN1 and its related cytokines IL‐1β, CCL5, and ICAM1 in oral lichen planus (OLP). Methods CCN1 expression levels in biopsies from OLP patients against normal oral mucosa (NOM) using immunohistochemistry (42 OLP vs 9 NOM) and RT‐qPCR (20 OLP vs 20 NOM) were compared, respectively. The correlation of CCN1 and IL‐1β, CCL5, and ICAM1 expression was examined by RT‐qPCR in tissue samples and an in vitro cell culture system using keratinocyte HaCaT cells incubated with lipopolysaccharides. Results Immunohistochemistry showed that CCN1 protein mainly expressed in the cytoplasm of epithelial keratinocytes of OLP. Consistently, RT‐qPCR revealed that mRNA expression of CCN1 was increased in OLP compared with NOM ( P < .05) and positively correlated with the high expression of IL‐1β, ICAM1, and CCL5 ( P < .001), respectively. Importantly, an in vitro study showed that keratinocyte proliferation significantly ( P < .05) increased by CCN1 stimulation. Moreover, IL‐1β, ICAM1, and CCL5 expression in keratinocytes stimulated by CCN1 was increased ( P < .05), respectively. Conclusions This preliminary study for the first time reported that altered expression of CCN1 was associated with high expression of IL‐1β, ICAM1, and CCL5 in OLP. And we demonstrated CCN1 promoted keratinocyte activation, as well as IL‐1β, ICAM1, and CCL5 production in keratinocytes. Our data indicated that the potential role of CCN1 and its related cytokines was involved in the pathogenesis of OLP.