請用此 Handle URI 來引用此文件：
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/63146完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 郭彥彬 | |
| dc.contributor.author | Jenny Zwei-Chieng Chang | en |
| dc.contributor.author | 張瑞青 | zh_TW |
| dc.date.accessioned | 2021-06-16T16:25:00Z | - |
| dc.date.available | 2023-01-21 | |
| dc.date.copyright | 2013-03-04 | |
| dc.date.issued | 2013 | |
| dc.date.submitted | 2013-01-22 | |
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Sedlaczek, N., et al., Proliferating bile duct epithelial cells are a major source of connective tissue growth factor in rat biliary fibrosis. Am J Pathol, 2001. 158(4): p. 1239-44. 172. Chen, M.M., et al., CTGF expression is induced by TGF- beta in cardiac fibroblasts and cardiac myocytes: a potential role in heart fibrosis. J Mol Cell Cardiol, 2000. 32(10): p. 1805-19. 173. Holmes, A., et al., CTGF and SMADs, maintenance of scleroderma phenotype is independent of SMAD signaling. J Biol Chem, 2001. 276(14): p. 10594-601. 174. Haydont, V., et al., Specific signals involved in the long-term maintenance of radiation-induced fibrogenic differentiation: a role for CCN2 and low concentration of TGF-beta1. Am J Physiol Cell Physiol, 2008. 294(6): p. C1332-41. 175. Shi-wen, X., et al., CCN2 is necessary for adhesive responses to transforming growth factor-beta1 in embryonic fibroblasts. J Biol Chem, 2006. 281(16): p. 10715-26. 176. Deng, Y., Arecoline-induced CCN2 expression in human buccal mucosal fibroblasts via TGF-β signaling pathway. PhD thesis, 2012. 177. Weng, H.L., et al., Profibrogenic transforming growth factor-beta/activin receptor-like kinase 5 signaling via connective tissue growth factor expression in hepatocytes. Hepatology, 2007. 46(4): p. 1257-70. 178. Thompson, K., D.W. Hamilton, and A. Leask, ALK5 inhibition blocks TGF-beta-induced CCN2 expression in gingival fibroblasts. J Dent Res, 2010. 89(12): p. 1450-4. 179. Bonniaud, P., et al., Progressive transforming growth factor beta1-induced lung fibrosis is blocked by an orally active ALK5 kinase inhibitor. Am J Respir Crit Care Med, 2005. 171(8): p. 889-98. 180. Higashiyama, H., et al., Inhibition of activin receptor-like kinase 5 attenuates bleomycin-induced pulmonary fibrosis. Exp Mol Pathol, 2007. 83(1): p. 39-46. 181. 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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/63146 | - |
| dc.description.abstract | 轉化生長因子β（transforming growth factor β；TGFβ）在口腔黏膜下纖維化症（OSF）中扮演了刺激膠原蛋白合成以及減少膠原蛋白分解因而加重纖維化的重要角色。結締組織生長因子（CTGF/CCN2）是轉化生長因子β下游基因產物，幾乎所有轉化生長因子β前纖維化作用和刺激細胞外間質蛋白合成的功能，都需要結締組織生長因子的共同參與。以檳榔鹼（arecoline）刺激人類頰黏膜纖維母細胞（BMFs）可以誘導人類頰黏膜纖維母細胞中結締組織生長因子與環氧酵素二型（cyclooxygenase-2；COX-2）表現。在口腔黏膜下纖維化症的組織中，可以發現結締組織生長因子與環氧酵素二型的過度表現。但是關於口腔黏膜中轉化生長因子β誘導結締組織生長因子表現的訊息傳遞路徑及環氧酵素二型對結締組織生長因子表現的影響仍不清楚。本研究主旨在研究以轉化生長因子β1刺激人類頰黏膜纖維母細胞誘導結締組織生長因子表現的訊息傳導路徑，冀望可以藉由抑制這些訊息傳導路徑成員來達到預防或治療口腔黏膜下纖維化症。我們發現使用TGFβ1 receptor ALK5抑制劑SB431542、Rac1抑制劑NSC23766 、JNK專一性抑制劑 SP600125、p38 MAPK專一性抑制劑SB203580、抗氧化劑N-acetylcysteine （NAC）、泛NOX抑制劑diphenyleneiodonium chloride （DPI）、NOX4抑制劑plumbagin、Src抑制劑 （PP2、Src inhibitor-1及 Src si-RNA）做前處理都可以明顯地減少人類頰黏膜纖維母細胞中TGFβ1誘導結締組織生長因子的表現。但ERK專一性抑制劑PD98059、NOX2抑制劑 apocynin 則沒有影響。進一步研究發現，NAC、DPI可以抑制 Src 的活化，但NSC23766 則沒有影響。NAC、DPI 、PP2可以抑制 JNK 的活化，但NSC23766 也沒有影響。NAC、DPI可以抑制 p38 MAPK 的活化，但NSC23766 、PP2沒有影響。NAC、PP2可以抑制 SMAD3 的活化，但NSC23766 、DPI沒有影響。結果顯示，人類頰黏膜纖維母細胞中TGFβ1誘導的結締組織生長因子表現至少經由四條路徑所調控，其分別為TGFβ1/ALK5/Rac1/CTGF(CCN2)、TGFβ1/ALK5/ROS/Src/SMAD3/CTGF、TGFβ1/ALK5/NOX4/ROS/Src/JNK/CTGF 和 TGFβ1/ALK5/NOX4/ROS/p38/CTGF 路徑。茶多酚 EGCG 藉由抑制 JNK 和 p38 MAPK 的磷酸化來阻斷TGFβ1誘導人類頰黏膜纖維母細胞產生的結締組織生長因子蛋白。前列腺素E2 （prostaglandin E2; PGE2）可以抑制人類肺細胞株IMR90中TGFβ1誘導的結締組織生長因子表現，但不能抑制人類頰黏膜纖維母細胞中TGFβ1誘導的結締組織生長因子表現。由於人類頰黏膜纖維母細胞中獨特的訊息傳導路徑致使前列腺素E2無法抑制結締組織生長因子表現以致在口腔黏膜下纖維化症組織中環氧酵素二型能與結締組織生長因子並存。最後發現EGCG亦可以抑制TGFβ1誘導人類頰黏膜纖維母細胞產生的第一型前膠原纖維蛋白表現、減少TGFβ1造成的膠狀膠原收縮、並且可以阻斷 TGFβ1引起的可溶性膠原蛋白的生成。因此茶多酚 EGCG 對於預防以及治療口腔黏膜下纖維化症將有很大的潛力。 | zh_TW |
| dc.description.abstract | Transforming growth factor β (TGFβ) has been suggested as the main trigger for the increased collagen production and decreased matrix degradation pathways in oral submucous fibrosis (OSF). Connective tissue growth factor (CTGF/CCN2) is required for most of the increased ECM production and other profibrotic activities generally observed in response to TGFβ. Arecoline induces CCN2 and cyclooxygenase-2 (COX-2) expressions in human buccal mucosal fibroblasts (BMFs). CTGF/CCN2 and COX-2 have been found to overexpress in OSF. However, the molecular mechanisms are not entirely clear. The aims of this study were to investigate the molecular mechanism underlying the TGFβ-induced CTGF/CCN2 expressions in human buccal mucosal fibroblasts (BMFs) and to identify the potential targets for drug intervention or chemoprevention of OSF. Pretreatment with activin receptor-like kinase 5 (ALK5) inhibitor SB431542, Rac1 inhibitor NSC23766, c-Jun NH2-terminal kinase (JNK) inhibitor SP600125, p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580, antioxidant N-acetyl-L-cysteine (NAC), NOX inhibitor diphenylene iodonium (DPI), NOX4 inhibitor plumbagin, and Src inhibitors (PP2, Src inhibitor-1, and Src si-RNA) significantly reduced TGFβ1-induced CTGF/CCN2 synthesis in BMFs, but not extracellular signal-regulated kinase (ERK) inhibitor PD98059, or NOX2 inhibitor apocynin. Furthermore, the phosphorylations of Src were inhibited by NAC and DPI but not NSC23766. The phosphorylations of JNK were inhibited by NAC, DPI, and PP2 but not NSC23766. The phosphorylations of p38 MAPK were inhibited by NAC and DPI but not NSC23766 or PP2. The phosphorylations of SMAD3 were inhibited by NAC and PP2 but not NSC23766 or DPI. These results revealed that multiple parallel signal transduction pathways together mediated the TGFβ1-induced CTGF/CCN2 expression in BMFs. At least four major pathways TGFβ1/ALK5/Rac1/CTGF(CCN2), TGFβ1/ALK5/ROS/Src/SMAD3/CTGF, TGFβ1/ALK5/NOX4/ROS/Src/JNK/CTGF, and TGFβ1/ALK5/NOX4/ROS/p38/CTGF were identified. Epigallocatechin-3-gallate (EGCG) blocked TGFβ1-induced CTGF/CCN2 synthesis by inhibiting the phosphorylation of Src, JNK, and p38 MAPK. Prostaglandin E2 (PGE2) inhibited the TGFβ1-induced CTGF/CCN2 synthesis in human fetal lung fibroblasts IMR90 but not in BMFs. The exceptional signal transduction pathways of TGFβ1-induced CTGF/CCN2 production in BMFs contribute to the resistance of PGE2 downregulation of CTGF/CCN2 expression; therefore, the CTGF/CCN2 levels are maintained in the OSF tissues in the presence of COX-2. In addition, EGCG inhibits the expression of TGFβ1-induced type I procollagen, reduces the excessive soluble collagens produced by TGFβ1-treated BMFs, and attenuates the fibroblast-mediated gel contraction stimulated by TGFβ1. Therefore, EGCG may serve as a useful agent in controlling OSF. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-16T16:25:00Z (GMT). No. of bitstreams: 1 ntu-102-D93422002-1.pdf: 4053355 bytes, checksum: 769ff3699319e6f0444697e3b794fd85 (MD5) Previous issue date: 2013 | en |
| dc.description.tableofcontents | TABLE OF CONTENTS
DEDICATIONS iii CHINESE ABSTRACT iv ENGLISH ABSTRACT vi INTRODUCTION 1 The epidemiology of oral submucous fibrosis 1 The habit of areca quid 1 The histopathological manifestations of oral submucous fibrosis 2 The pathogenesis of oral submucous fibrosis 3 Management of oral submucous fibrosis 3 The molecular mechanisms regarding pathogenesis of OSF 4 Transforming growth factor-beta (TGFβ) versus fibrotic pathologies 7 Connective tissue growth factor (CTGF/CCN2) versus TGFβ 9 The transforming growth factor-beta (TGFβ) signaling 12 The role of reactive oxygen species (ROS) in fibrosis 14 The role of NADPH oxidase (NOX) in fibrosis 16 The Src family kinases vesus TGFβ signaling 18 The antifibrogenic effects of epigallocatechin-3-gallate (EGCG) 20 PURPOSE 25 MATERIALS AND METHODS 27 Materials 27 Cell culture 28 Western blot analysis 29 Src siRNA transfection 29 Quantitative real-time polymerase chain reaction (qRT-PCR) 30 Fibroblast-populated collagen lattices (FPCL) 31 Sircol soluble collagen assay 31 Statistical analysis 32 RESULTS 33 TGFβ1 stimulated CTGF/CCN2 expression in buccal mucosal fibroblasts (BMFs) 33 PGE2 could NOT inhibit the TGFβ1-induced CTGF/CCN2 in BMFs 33 ALK5, JNK, and p38 MAPK were involved in the TGFβ1-induced CTGF/CCN2 33 EGCG attenuated the TGFβ1-induced phosphorylation of JNK and p38 34 EGCG abrogated the TGFβ1-induced procollagen alpha-1 type I 35 EGCG decreased the TGFβ1-stimulated production of soluble collagens 35 EGCG attenuated the TGFβ1-stimulated collagen gel contraction 36 NOX4 and ROS are involved in the TGFβ1-induced CTGF/CCN2 in BMFs 36 Src played a role in the TGFβ1-induced CTGF/CCN2 in BMFs 37 Src was downstream of ROS and upstream of JNK and SMAD3 38 DISCUSSION 40 CONCLUSIONS 49 FIGURES 51 REFERENCES 70 APPENDIX 1 88 APPENDIX 2 94 | |
| dc.language.iso | en | |
| dc.subject | 結締組織生長因子 | zh_TW |
| dc.subject | 茶多酚 | zh_TW |
| dc.subject | CTGF/CCN2 | zh_TW |
| dc.subject | 口腔黏膜下纖維化症 | zh_TW |
| dc.subject | 轉化生長因子β | zh_TW |
| dc.subject | Transforming growth factor β | en |
| dc.subject | Connective tissue growth factor | en |
| dc.subject | EGCG | en |
| dc.subject | Oral submucous fibrosis | en |
| dc.subject | TGFβ1 | en |
| dc.subject | CTGF/CCN2 | en |
| dc.title | TGFβ1經由 NOX4/Src 訊息傳遞路徑誘導人類頰黏膜纖維母細胞結締組織生長因子表現 | zh_TW |
| dc.title | TGFβ1-induced CTGF/CCN2 expression in human buccal mucosal fibroblasts via NOX4/Src signaling pathway | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 101-1 | |
| dc.description.degree | 博士 | |
| dc.contributor.oralexamcommittee | 江俊斌,張國威,張育超,周涵怡 | |
| dc.subject.keyword | 結締組織生長因子,茶多酚,口腔黏膜下纖維化症,轉化生長因子β,CTGF/CCN2, | zh_TW |
| dc.subject.keyword | CTGF/CCN2,Connective tissue growth factor,EGCG,Oral submucous fibrosis,TGFβ1,Transforming growth factor β, | en |
| dc.relation.page | 101 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2013-01-22 | |
| dc.contributor.author-college | 牙醫專業學院 | zh_TW |
| dc.contributor.author-dept | 臨床牙醫學研究所 | zh_TW |
| 顯示於系所單位： | 臨床牙醫學研究所 | |
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