The Research of B7-H1 Expression in Oral Submucous Fibrosis

• Main Authors: Chia-Yin Chin, 秦嘉霠
• Other Authors: Hsin-Ming Chen
• Format: Others
• Language: zh-TW
• Published: 2012
• Online Access: http://ndltd.ncl.edu.tw/handle/31586246889627902355

碩士 === 國立臺灣大學 === 口腔生物科學研究所 === 100 === Oral submucous fibrosis is a continuous, chronic, insidious and inflammatory disease of oral mucous that is a kind of potentially malignant disorders. OSF is mainly due to consumed areca quid which is lead to fibrosis in the oral cavity. In the progression of inflammatory, some pro-inflammatory and pro-fibrotic cytokine could be upregulated, like TGF-β、IFN-γ, etc., the exact pathogenesis of OSF and cytokine was still unclear and needed to study .However, the previously study had showed that B7-H1 was regulated by IFN-γ in the human dermal fibroblast. Therefore, in this study, we investigated whether B7-H1 was involved in the mechanisms of OSF diseases. First, we investigated the expression of B7-H1 in normal oral mucosa tissue and in OSF patient’s tissue by immunohistochemistry (IHC).The result showed that most of fibroblasts that express B7-H1 was close to epithelium layer in OSF tissue. It also showed that the expression of B7-H1 in epithelium layer in OSF is much more than in NOM. Then, we treated NOM fibroblast with arecoline and analyzed the expression of B7-H1 by Western blot. The result showed that B7-H1 is up-regulated by arecoline in NOM, and JNK inhibitor could reduce B7-H1 expression. The reference indicated that B7-H1 over-expression could be regulated Epithelial-mesenchymal transition (EMT) in human skin cancer. The result of IHC showed that fibroblasts that express B7-H1 were in the juxta-epithelial connective tissue. The reference showed that EMT is one of important mechanisms of OSF, and to investigate whether B7-H1 is involved in EMT which is lead to fibrosis. We treated S-G epithelial cell with TGF-β, and the result showed that EMT biomarker protein and B7-H1 expression was increased. And then, we pre-treat S-G cell with JNK inhibitor and then treat with TGF-β, the result showed that the expression of B7-H1 and some EMT biomarker both were reduced. And then, we used B7-H1 specific siRNA to knockdown its expression in S-G cells. The result showed that knockdown of expression of B7-H1 influenced EMT biomarker gene expression.