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    Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/2885


    Title: 第一型胞漿素原活化抑制劑基因在口腔黏膜下纖維化症的表現
    The Eexpression of Type I Plasminogen Activator Inhibitor Gene in Oral Submucous Fibrosis
    Authors: 張育超;周明勇;謝易修
    Chang, Yu-Chao;Chou, Ming-Yung;Hsieh, Yih-Shou
    Contributors: 中山醫學院牙醫學系
    Keywords: 口腔黏膜下纖維化症;胞漿素原活化抑制劑;口腔黏膜;纖維化;基因表現
    Oral submucous fibrosis;Plasminogen activator inhibitor;Oral mucosa;Fibrosis;Gene expression
    Date: 2003
    Issue Date: 2010-11-25T03:43:12Z (UTC)
    Abstract: Objective: Oral submucous fibrosis (OSF) is a pre-malignant fibrotic lesion of the mouth in areca quid chewers. It is probably a consequence of disturbances in the hemeostatic equilibrium between synthesis and degradation of extracellular matrix molecules. Recently, we found that plasminogen activator inhibitor-1 (PAI-1) mRNA and protein were be upregulation in OSF (Oral Oncology 2003:367?V72). However, the detailed molecular mechanism is stilled remained to be elucidated. Methods: In this study, we investigated the genetic analysis of PAI-1 in the upstream -675bp of the promoter region between OSF and normal buccal mucosa. PAI-1 genotyping with allele-specific restriction enzyme site analysis was performed in the specimens from 52 OSF and 32 normal buccal mucosa. The Chi-square test was used as statistical analysis in this study. Results: There is a single guanosine deletion/insertion 4G/5G polymorphism -675 bp upstream from the start of transcription within the promoter. Our findings suggested that the distribution pattern of PAI-1 promoter were different between OSF and normal buccal mucosa (P< 0.05). It had a high frequency of PAI-1 (4G/4G) genotypes in the OSF group (42.3%) than those in normal buccal mucosa group (21.9%). The ratio of 4G/5G from OSF and normal buccal mucosa were 44.2% and 46.9%. In addition, the ratio of 5G/5G was 13.5%, 31.2% respectively. Conclusions: We concluded the results that PAI-1 4G allele, with a higher transcription activity, was more prevalent in OSF. This may be the molecular mechanism associated with an increased risk for OSF.
    URI: https://ir.csmu.edu.tw:8080/handle/310902500/2885
    Appears in Collections:[牙醫學系暨碩士班] 研究計劃

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