HDAC-2 expression in oral submucous fibrosis and its possible pathogenesis and mechanism

碩士 === 國立臺灣大學 === 口腔生物科學研究所 === 95 === ABSTRACT Oral submucous fibrosis (OSF) is a chronic debilitating disease and a pre-malignant condition of the oral cavity. It is characterized by a generalized submucous fibrosis. Epidemiological evidences strongly indicate the association of the areca quid (A...

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Main Authors: Ming-Fan Tsai, 蔡旻汎
Other Authors: 陳信銘
Format: Others
Language:zh-TW
Published: 2007
Online Access:http://ndltd.ncl.edu.tw/handle/94416589118180354587
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spelling ndltd-TW-095NTU055960062015-12-07T04:04:29Z http://ndltd.ncl.edu.tw/handle/94416589118180354587 HDAC-2 expression in oral submucous fibrosis and its possible pathogenesis and mechanism 口腔黏膜下纖維化症中HDAC-2表現及可能致病機轉之研究 Ming-Fan Tsai 蔡旻汎 碩士 國立臺灣大學 口腔生物科學研究所 95 ABSTRACT Oral submucous fibrosis (OSF) is a chronic debilitating disease and a pre-malignant condition of the oral cavity. It is characterized by a generalized submucous fibrosis. Epidemiological evidences strongly indicate the association of the areca quid (AQ) habit and OSF. It is regarded as a pre-cancerous condition. HDAC-2 (Histone deacetylase H2) has been evidenced to have over expression in some organs, such as lung, liver, and skin, but the underlying mechanisms remain to be clarified. In our study, we will discuss the pathogenesis between the severity of Oral submucous fibrosis (OSF) and the expression of HDAC-2 (Histone deacetylase H2). In the beginning, we collect 59 OSF specimens and 15 normal buccal mucosa that were examined the expression of HDAC-2 by immunohistochemistry (IHC). All patients received surgical excision of their precancerous at the Department of Oral and Maxillofacial Surgery, National Taiwan University Hospital, Taipei, Taiwan. The results of this study showed the HDAC-2 positive rate of OSF is significantly higher than that of normal oral mucosa (NOM) (P=0.0045).The incident rate of the OSF(ICR=96.6%)specimens, HDAC-2 is strongly expressed in the fibroblasts of connective tissue more than normal buccalmucosa(ICR=13.3%)specimens. In addition, the expression of HDAC-2 protein between OSF and NOM was quantified with the use of Western blotting and the results showed the same with IHC assay. Besides, SAHA (suberoylanilide hydroxamic acid) an HDAC-2 inhibitor was added to find the effect on OSF and NOM in a time- dependent manner by western blotting assay. And our studied indicated that after we added the SAHA for 12 hours this inhibitor is markedly reduced the expression of HDAC-2, especially in OSF (p<0.05). In other word, we can see the result suggests that In the OSF , HDAC-2 is strongly expressed in the fibroblasts of connective tissue protein more than normal buccal mucosa. And the result finds that HDAC-2 is higher expression and harder to be repressed in the OSF than in the NOM. Hence, the result suggests that over deposition of collagen maybe related to the over expression and hard to be repressed of HDAC-2 in the OSF. 陳信銘 2007 學位論文 ; thesis 61 zh-TW
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language zh-TW
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description 碩士 === 國立臺灣大學 === 口腔生物科學研究所 === 95 === ABSTRACT Oral submucous fibrosis (OSF) is a chronic debilitating disease and a pre-malignant condition of the oral cavity. It is characterized by a generalized submucous fibrosis. Epidemiological evidences strongly indicate the association of the areca quid (AQ) habit and OSF. It is regarded as a pre-cancerous condition. HDAC-2 (Histone deacetylase H2) has been evidenced to have over expression in some organs, such as lung, liver, and skin, but the underlying mechanisms remain to be clarified. In our study, we will discuss the pathogenesis between the severity of Oral submucous fibrosis (OSF) and the expression of HDAC-2 (Histone deacetylase H2). In the beginning, we collect 59 OSF specimens and 15 normal buccal mucosa that were examined the expression of HDAC-2 by immunohistochemistry (IHC). All patients received surgical excision of their precancerous at the Department of Oral and Maxillofacial Surgery, National Taiwan University Hospital, Taipei, Taiwan. The results of this study showed the HDAC-2 positive rate of OSF is significantly higher than that of normal oral mucosa (NOM) (P=0.0045).The incident rate of the OSF(ICR=96.6%)specimens, HDAC-2 is strongly expressed in the fibroblasts of connective tissue more than normal buccalmucosa(ICR=13.3%)specimens. In addition, the expression of HDAC-2 protein between OSF and NOM was quantified with the use of Western blotting and the results showed the same with IHC assay. Besides, SAHA (suberoylanilide hydroxamic acid) an HDAC-2 inhibitor was added to find the effect on OSF and NOM in a time- dependent manner by western blotting assay. And our studied indicated that after we added the SAHA for 12 hours this inhibitor is markedly reduced the expression of HDAC-2, especially in OSF (p<0.05). In other word, we can see the result suggests that In the OSF , HDAC-2 is strongly expressed in the fibroblasts of connective tissue protein more than normal buccal mucosa. And the result finds that HDAC-2 is higher expression and harder to be repressed in the OSF than in the NOM. Hence, the result suggests that over deposition of collagen maybe related to the over expression and hard to be repressed of HDAC-2 in the OSF.
author2 陳信銘
author_facet 陳信銘
Ming-Fan Tsai
蔡旻汎
author Ming-Fan Tsai
蔡旻汎
spellingShingle Ming-Fan Tsai
蔡旻汎
HDAC-2 expression in oral submucous fibrosis and its possible pathogenesis and mechanism
author_sort Ming-Fan Tsai
title HDAC-2 expression in oral submucous fibrosis and its possible pathogenesis and mechanism
title_short HDAC-2 expression in oral submucous fibrosis and its possible pathogenesis and mechanism
title_full HDAC-2 expression in oral submucous fibrosis and its possible pathogenesis and mechanism
title_fullStr HDAC-2 expression in oral submucous fibrosis and its possible pathogenesis and mechanism
title_full_unstemmed HDAC-2 expression in oral submucous fibrosis and its possible pathogenesis and mechanism
title_sort hdac-2 expression in oral submucous fibrosis and its possible pathogenesis and mechanism
publishDate 2007
url http://ndltd.ncl.edu.tw/handle/94416589118180354587
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