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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/61893完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 林琬琬 | |
| dc.contributor.author | Nan-Lin Wu | en |
| dc.contributor.author | 吳南霖 | zh_TW |
| dc.date.accessioned | 2021-06-16T13:17:33Z | - |
| dc.date.available | 2015-09-24 | |
| dc.date.copyright | 2013-09-24 | |
| dc.date.issued | 2013 | |
| dc.date.submitted | 2013-07-27 | |
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Otsuki, T., Tomokuni, A., Sakaguchi, H., Aikoh, T., Matsuki, T., Isozaki, Y., Hyodoh, F., Ueki, H., Kusaka, M., Kita, S., and Ueki, A. (2000). Over-expression of the decoy receptor 3 (DcR3) gene in peripheral blood mononuclear cells (PBMC) derived from silicosis patients. Clin Exp Immunol 119, 323-327. Papp, H., Czifra, G., Lazar, J., Gonczi, M., Csernoch, L., Kovacs, L., and Biro, T. (2003). Protein kinase C isozymes regulate proliferation and high cell density-mediated differentiation in HaCaT keratinocytes. Experimental dermatology 12, 811-824. Pastore, S., Mascia, F., Mariani, V., and Girolomoni, G. (2008). The epidermal growth factor receptor system in skin repair and inflammation. J Invest Dermatol 128, 1365-1374. Peternel, S., Prpic-Massari, L., Manestar-Blazic, T., Brajac, I., and Kastelan, M. (2011). Increased expression of TRAIL and its death receptors DR4 and DR5 in plaque psoriasis. Arch Dermatol Res 303, 389-397. 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Scott, K.A., Arnott, C.H., Robinson, S.C., Moore, R.J., Thompson, R.G., Marshall, J.F., and Balkwill, F.R. (2004). TNF-alpha regulates epithelial expression of MMP-9 and integrin alphavbeta6 during tumour promotion. A role for TNF-alpha in keratinocyte migration? Oncogene 23, 6954-6966. Sebastian, S., Settleman, J., Reshkin, S.J., Azzariti, A., Bellizzi, A., and Paradiso, A. (2006). The complexity of targeting EGFR signalling in cancer: from expression to turnover. Biochim Biophys Acta 1766, 120-139. Sedger, L.M., Glaccum, M.B., Schuh, J.C., Kanaly, S.T., Williamson, E., Kayagaki, N., Yun, T., Smolak, P., Le, T., Goodwin, R., and Gliniak, B. (2002). Characterization of the in vivo function of TNF-alpha-related apoptosis-inducing ligand, TRAIL/Apo2L, using TRAIL/Apo2L gene-deficient mice. Eur J Immunol 32, 2246-2254. Segre, J.A. (2006). Epidermal barrier formation and recovery in skin disorders. J Clin Invest 116, 1150-1158. Shepard, H.M., Brdlik, C.M., and Schreiber, H. (2008). Signal integration: a framework for understanding the efficacy of therapeutics targeting the human EGFR family. J Clin Invest 118, 3574-3581. Shirakata, Y., Komurasaki, T., Toyoda, H., Hanakawa, Y., Yamasaki, K., Tokumaru, S., Sayama, K., and Hashimoto, K. (2000). Epiregulin, a novel member of the epidermal growth factor family, is an autocrine growth factor in normal human keratinocytes. J Biol Chem 275, 5748-5753. Song, J.J., and Lee, Y.J. (2008). Differential cleavage of Mst1 by caspase-7/-3 is responsible for TRAIL-induced activation of the MAPK superfamily. Cell Signal 20, 892-906. Stoll, S.W., Kansra, S., Peshick, S., Fry, D.W., Leopold, W.R., Wiesen, J.F., Sibilia, M., Zhang, T., Werb, Z., Derynck, R., Wagner, E.F., and Elder, J.T. (2001). Differential utilization and localization of ErbB receptor tyrosine kinases in skin compared to normal and malignant keratinocytes. Neoplasia 3, 339-350. Strasser, A., Jost, P.J., and Nagata, S. (2009). T | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/61893 | - |
| dc.description.abstract | 皮膚是人體的第一線障壁，可防止過量水份經皮喪失，並保護個體免於受到外來的傷害及病原體的入侵。皮膚角質細胞的持續增生與控制良好的細胞死亡過程之間能否平衡對於正常皮膚的恆定性是重要的。角質化是皮膚角質細胞終端分化的過程，是一種與細胞凋亡有所不同的特殊性的計畫性細胞死亡。這些終端分化的死亡角質細胞將會建構皮膚最外層的角質層，作為皮膚主要的障壁。而皮膚內各種不同細胞包括上皮角質細胞、真皮纖維母細胞、及各種免疫細胞之間的協調作用對於維持皮膚的恆定性也是不可或缺的。當正常皮膚恆定性受到破壞時，將會造成各種細胞異常增生、死亡，分化異常以及嚴重發炎的皮膚疾病。上皮角質細胞如同免疫細胞一樣，也會表現許多腫瘤壞死因子家族成員及受體。雖然許多表現在免疫細胞的家族成員及受體的生物功能已被發現，但是許多腫瘤壞死因子家族成員及受體在皮膚的生物角色仍然所知有限。
在我們的研究中，我們首先評估tumor necrosis factor related apoptosis-inducing ligand (TRAIL) 對上皮角質細胞的作用。TRAIL 是一種廣為人知可誘發變異細胞產生細胞凋亡的因子，而我們主要著重於TRAIL對於角質細胞終端分化的作用及其潛在的分子機轉。在第二部分，我們則研究第三號誘餌受體在乾癬的表現。乾癬是一種角質細胞增生及分化異常、發炎及血管新生的皮膚疾病。第三號誘餌受體是Fas ligand (FasL)，LIGHT (TNFSF14) 及TNF-like molecule 1A (TL1A) 的游離受體，在許多發炎疾病、自體免疫疾病及惡性疾病的致病過程中扮演了多重角色。在皮膚生物學方面，第三號誘餌受體已被發現可表現於皮膚初始角質細胞；而且在乾癬皮膚病灶中，第三號誘餌受體的表現會上升。然而第三號誘餌受體在乾癬皮膚病灶的表現是如何被調控的，目前仍然未知。 在第一部分中，我們發現TRAIL可誘發角質細胞表現終端分化標誌如involucrin 及 type 1 transglutaminase。TRAIL誘導角質細胞分化時，caspases 3 及 8會活化，同時間細胞凋亡也會被誘發。抑制這些凋亡性caspase會同時抑制TRAIL所誘發的細胞凋亡與終端分化，但是卻不太會影響鈣及phorbol 12-myristate 13-acetate所誘導的角質細胞分化現象。並且TRAIL也會差別性調控角質細胞ERK及p38的活化現象。此外，TRAIL所活化的caspase會造成p63的降解，然而p63的存在對於TRAIL誘導角質細胞分化是必須的，因為knock down ΔNp63會減少TRAIL誘導的角質細胞分化。我們的結果顯示TRAIL可誘導角質細胞的分化及凋亡，而caspase關鍵性地調控這些過程。我們的研究提出了凋亡性caspase對角質細胞終端分化的一個新角色，也進一步闡明此特殊細胞死亡模式的分子機轉。 在第二部分裡，我們發現第三號誘餌受體可表現在乾癬皮膚病灶的真皮血管內皮細胞及病灶上皮組織。血清實驗分析顯示，相較於健康個體，乾癬病人的血清中有較高的第三號誘餌受體及較低的FasL。進一步的研究發現，表皮生長因子受體對於調控第三號誘餌受體在角質細胞的表現具有關鍵的角色。利用表皮生長因子及transforming growth factor (TGF)-alpha來活化表皮生長因子受體可明顯地促進角質細胞產生第三號誘餌受體。而與乾癬致病機轉有關的發炎性細胞激素中，腫瘤壞死因子alpha能增加角質細胞及血管內皮細胞產生第三號誘餌受體。此外，knock down表皮生長因子受體的表現及利用表皮生長因子受體抑制劑可以抑制腫瘤壞死因子alpha所誘發的第三號誘餌受體在角質細胞的表現。而NF-kappa B 路徑則關鍵性地參與了腫瘤壞死因子alpha及表皮生長因子作用的分子機轉。我們的研究結果闡明了第三號誘餌受體在角質細胞及內皮細胞表現的新穎調控機制，同時提供了乾癬致病機轉研究的新觀點。 | zh_TW |
| dc.description.abstract | Skin provides the primary barrier to prevent excessive water loss and protect against the external insults and invasion of pathogens. The homeostasis of normal skin is maintained by the balance between continuous replenishment of proliferating keratinocytes and well-controlled cell death. Cornification, the process of terminal differentiation of epidermal keratinocytes, is a special form of programmed cell death in skin and distinct from apoptotic cell death. These terminally differentiated, dead keratinocytes construct the outermost cornified layer, which is the principal barrier of skin. Skin homeostasis is also controlled by coordination between different cellular effectors in skin including epidermal keratinocytes, dermal fibroblasts and various immunocytes. Disturbance of skin homeostasis can lead to diverse disorders characterized by aberrant growth, cell death, differentiation or severe inflammation. Like immunocytes, epidermal keratinocytes also can express many members of tumor necrosis factor (TNF) and tumor necrosis factor receptor (TNFR) superfamily. Although many functions of TNF and TNFR superfamily in immune cells have been revealed, the known biological roles in skin still remain limited.
In our studies, we first tried to evaluate the effect of tumor necrosis factor related apoptosis-inducing ligand (TRAIL), which is a well-known apoptosis inducer in transformed cells, on primary human epidermal keratinocytes, focusing on keratinocyte differentiation and the underlying molecular mechanisms. Secondly, we investigated the expression of decoy receptor 3 (DcR3) in psoriasis, which is characterized by aberrant keratinocyte proliferation and differentiation, inflammation, and angiogenesis. DcR3 is a soluble receptor of Fas ligand (FasL), LIGHT (TNFSF14) and TNF-like molecule 1A (TL1A), and plays pleiotropic roles in many inflammatory and autoimmune disorders and malignant diseases. In cutaneous biology, DcR3 is expressed in primary human epidermal keratinocytes and is up-regulated in skin lesions of psoriasis. However, the regulatory mechanisms of DcR3 over-expression in skin lesions of psoriasis are unknown. For the part I, we found TRAIL could induce the expression of keratinocyte differentiation markers involucrin and type 1 transglutaminase in normal human epidermal keratinocytes. The induction of differentiation occurred mainly under the activation of caspases 3 and 8, and apoptosis could also be triggered. Inhibition of these apoptotic caspases attenuated both of the apoptosis and differentiation of keratinocytes caused by TRAIL, but barely affected the induction of differentiation caused by calcium and phorbol 12-myristate 13-acetate. The differential regulation of ERK and p38 activation by TRAIL was also observed. Moreover, the degradation of p63 was induced by TRAIL-elicited caspase activation. However, the existence of p63 is essential for the initiation of keratinocyte differentiation caused by TRAIL because knockdown of ΔNp63 decreased the TRAIL-induced differentiation. Taken together, our results suggest that TRAIL can be an inducer of both differentiation and apoptosis in human keratinocytes, and that caspases critically mediate these processes. This study identifies a new role of apoptotic caspases for terminal differentiation of keratinocytes and further elucidates the molecular pathways involved in this unique model of cell death. For part II, we demonstrate that DcR3 can be detected in both dermal blood vessels and epidermal layers of psoriatic skin lesions. Analysis of serum samples showed that DcR3 was elevated, but FasL was downregulated in psoriatic patients compared with normal individuals. Additional studies revealed a central role of epidermal growth factor receptor (EGFR) in controlling the basal expression of DcR3 in keratinocytes. Activation of EGFR by epidermal growth factor (EGF) or transforming growth factor (TGF)-alpha strikingly upregulated DcR3 production. TNF-alpha enhanced DcR3 expression in both keratinocytes and endothelial cells compared with various inflammatory cytokines involved in psoriasis. Additionally, TNF-alpha-enhanced DcR3 expression in keratinocytes was inhibited when EGFR was knocked down or EGFR inhibitor was used. The NF-kappa B pathway was critically involved in the molecular mechanisms underlying the action of EGFR and TNF-alpha. Collectively, the novel regulatory mechanisms of DcR3 expression in keratinocytes and endothelial cells provide new insights into the pathogenesis of psoriasis. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-16T13:17:33Z (GMT). No. of bitstreams: 1 ntu-102-D94443002-1.pdf: 8280422 bytes, checksum: 09c391823cadf3f19daee5705c6b88e2 (MD5) Previous issue date: 2013 | en |
| dc.description.tableofcontents | Table of contents
Abbreviations---------------------------------------------1 Abstract--------------------------------------------------4 中文摘要--------------------------------------------------7 Introduction------------------------------------------9 Specific Aims--------------------------------------------29 Materials and Methodsmm----------------------------------30 Part I: TRAIL-induced keratinocyte differentiation requires caspase activation and p63 expression Results--------------------------------------------------40 Discussion-----------------------------------------------46 Figures--------------------------------------------------52 Part II: EGFR-driven up-regulation of decoy receptor 3 in keratinocytes contributes to the pathogenesis of psoriasis Results--------------------------------------------------66 Discussion-----------------------------------------------74 Figures--------------------------------------------------80 Appendix-------------------------------------------------92 References-----------------------------------------------99 Publication---------------------------------------------129 | |
| dc.language.iso | en | |
| dc.subject | 角質細胞 | zh_TW |
| dc.subject | 分化 | zh_TW |
| dc.subject | 乾癬 | zh_TW |
| dc.subject | TRAIL | zh_TW |
| dc.subject | 表皮生長因子受體 | zh_TW |
| dc.subject | 第三號誘餌受體 | zh_TW |
| dc.subject | EGFR | en |
| dc.subject | DcR3 | en |
| dc.subject | keratinocyte | en |
| dc.subject | differentiation | en |
| dc.subject | psoriasis | en |
| dc.subject | TRAIL | en |
| dc.title | TRAIL及第三號誘餌受體在皮膚角質細胞終端分化及發炎疾病的角色探討 | zh_TW |
| dc.title | Roles of TRAIL and decoy receptor 3 in epidermal keratinocyte terminal differentiation and inflammatory skin diseases | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 101-2 | |
| dc.description.degree | 博士 | |
| dc.contributor.oralexamcommittee | 謝世良,許秉寧,符文美,王莉芳 | |
| dc.subject.keyword | TRAIL,第三號誘餌受體,角質細胞,分化,乾癬,表皮生長因子受體, | zh_TW |
| dc.subject.keyword | TRAIL,DcR3,keratinocyte,differentiation,psoriasis,EGFR, | en |
| dc.relation.page | 129 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2013-07-29 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 藥理學研究所 | zh_TW |
| 顯示於系所單位： | 藥理學科所 | |
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