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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/29789完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 張智芬 | |
| dc.contributor.author | Wen-Ling Chou | en |
| dc.contributor.author | 周玟伶 | zh_TW |
| dc.date.accessioned | 2021-06-13T01:18:55Z | - |
| dc.date.available | 2007-08-08 | |
| dc.date.copyright | 2007-08-08 | |
| dc.date.issued | 2007 | |
| dc.date.submitted | 2007-07-19 | |
| dc.identifier.citation | [1] E.E. Kershaw, J.S. Flier. (2004) Adipose tissue as an endocrine organ. J Clin Endocrinol Metab 89, 2548-2556.
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/29789 | - |
| dc.description.abstract | 3T3-L1 細胞株是一個研究脂肪細胞分化機制最常用的模式系統，本論文中，前列腺素還原酉每(PGR-2)最初是一個利用mRNA差異呈現法(differential display)，被篩選出來的一個功能未知的基因；它是一個在3T3-L1 的脂肪細胞分化過程後期高度表現的基因，在組織的分布上，尤其在脂肪組織中具有特別高的表現。經過基因庫序列的比對分析，基因的選殖及其重組蛋白質的表現，酵素活性的測試，以及酵素反應產物的定性分析，從而證實此基因的表現具有催化15-keto prostaglandin E2 (15-keto-PGE2)還原成為13,14-dihydro-15-ketoprostaglandin E2的15-oxoprostaglandin- Δ13-reductase酵素活性，也因此將此基因定名為前列腺素還原酉每(PGR-2)。
前列腺素E2是一個半生期很短的活性小分子，其分解代謝先由 NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH)進行氧化反應產生15-keto-PGE2，再由NADPH/NADH-dependent 15-oxoprostaglandin-Δ13-reductase(PGR)進一步還原作用將15-keto-PGE2轉變為沒有活性的 13,14-dihydro-15-keto-PGE2。早期的研究發現脂肪組織具有高度的PGDH 與PGR之酵素活性，顯示前列腺素E2分解代謝在脂肪細胞中是旺盛的。 PPAR-γ 是一個在調控脂肪細胞分化上扮演重要角色的轉錄因子，在轉錄因子的分類上，它是屬於nuclear receptor的子家族成員，配體(ligand)對PPAR-γ的結合，使得轉錄輔抑制子從而脫離，並促使轉錄輔活化子返回與PPAR-γ結合，同時PPAR-γ藉由與retinoid X receptor (RXR)形成異二聚體才能進而活化其標的基因。目前臨床上治療糖尿病的藥物thiazolidinedione(TZD)，即是一類化學合成的PPAR-γ高親合性配體；過去一些天然的化學分子已被報導為潛在的內生性PPAR-γ的配體，但在生理上這些配體是否確實活化PPAR-γ則仍然沒有定論，有趣的是這些天然的化學分子往往伴隨不同的發炎刺激而產生，這與PPAR-γ日益明朗的抗發炎角色呈現正相關性。前列腺素E2的生成在許多發炎反應中皆會明顯增加，然而其代謝是否與調節PPAR-γ活性有關仍屬未知的議題。 本論文中，在3T3-L1 的細胞分化前期額外表現PGR-2 蛋白質時，脂肪細胞的分化明顯被抑制，但卻不影響分化前期PPAR-γ蛋白質的表現；然後，我進一步發現15-keto-PGE2是一個PPAR-γ的配體，藉由增進PPAR-γ與轉錄輔活化子的結合，而活化PPAR-γ的轉錄功能，使其能有效促進PPAR-γ標的基因的表現，與3T3-L1 的脂肪細胞分化；在293T細胞中，以轉染實驗表現PGR-2 蛋白質，的確能夠抑制15-keto-PGE2所引發的PPAR-γ的轉錄活化，反之，以轉染實驗表現前列腺素脫氫酉每15-hydroxyprostaglandin dehydrogenase (PGDH)蛋白質，使其氧化PGE2成為15-keto-PGE2，的確能夠促進PPAR-γ的轉錄活化。因此，根據以上的研究成果，我們認為細胞內PGE2的分解代謝，在調節PPAR-γ的轉錄活化的機制中，可能扮演一個重要的角色。 | zh_TW |
| dc.description.abstract | 3T3-L1 preadipocyte cell line has been used as a model for characterizing the events responsible for adipocyte differentiation. In this thesis, we used differential display to identify a novel gene, encoding prostaglandin reductase designated as PGR-2, in the beginning. Its expression pattern is abundant in adipose tissues and highly up-regulated in the late phase of 3T3-L1 adipocyte differentiation. By functional characterization, we found that PGR-2 is capable of converting 15-keto-PGE2 into 13,14-dihydro-15-keto-PGE2.
PGE2, a short lived mediator, is catabolized via an oxidation reaction catalyzed by NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) for the generation of 15-keto-PGE2, which is further catabolized by a reduction reaction catalyzed by NADPH/NADH-dependent 15-oxoprostaglandin-Δ13-reductase (PGR). It has been shown that adipose tissue possesses high activity of both PGDH and PGR, indicating that PGE2 catabolism is highly active in adipocytes. Peroxisome proliferator-activated receptor γ (PPAR-γ) plays important roles in adipogenesis. PPAR-γ is a ligand-dependent transcription factor that belongs to the nuclear receptor family, activating the transcription of its target genes as heterodimers with retinoid X receptor (RXR). Upon ligand binding, PPAR-γreleases bound corepressors and recruits coactivator for transcriptional activation. Thiazolidinediones (TZDs) are high-affinity synthetic agonists which have been widely used as insulin-sensitizing agents to treat type 2 diabetes. Several natural substances have been identified as potential endogenous PPAR-γ ligands. To date, their physiological significance and role as true endogenous activators for PPAR-γ have been uncertain. Interestingly, these identified ligands are usually associated with different inflammatory stimuli, which correlate with the anti-inflammatory role of PPAR-γ. The production of prostaglandin E2 (PGE2) is elevated in many inflammatory stimuli. However, little is known about whether the catabolism of PGE2 is associated with modulation of PPAR-γactivity. In this thesis, enforced expression of PGR-2 represses transcriptional activity of PPAR-γand adipocyte differentiation of 3T3-L1 cells. Following these observations, we further found that 15-keto-PGE2, an intermediate metabolite within the PGE2 catabolic pathway, functions as a PPAR-γ ligand, by which it stimulates the differentiation of mouse fibroblasts into adipocytes. In accordance, overexpression of PGDH also increased PGE2-dependent activation of PPAR-γ. Our findings provide new insights into PGE2 catabolism in regulation of PPAR-γactivity. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-13T01:18:55Z (GMT). No. of bitstreams: 1 ntu-96-D90442002-1.pdf: 3443618 bytes, checksum: 11f7a9a78fd793dafe273a134356b511 (MD5) Previous issue date: 2007 | en |
| dc.description.tableofcontents | 口試委員會審定書 I
謝誌 II 中文摘要 IV Abstract VI Chapter I. Overview the hormonal signaling and transcriptional control of adipocyte differentiation. ……………………………………………………………………1 1. Physiological roles of adipose tissues 1.1 Overview 1.2 Adipose tissue as an endocrine organ 1.3 Obesity and energy balance 2. Program of adipose development 2.1 Commitment of multipotent stem cell to the adipocyte lineage 2.2 Terminal differentiation of adipocytes 3. Transcription control of adipocyte differentiation 3.1 Overview 3.2 C/EBP-β and -δ 3.3 PPAR-γ 3.4 C/EBP-α 3.5 ADD1/SREBP-1c 3.6 Other transcription factors 4. Cellular and hormonal regulation of adipogenesis 4.1 Factors that stimulate adipogenesis 4.2 Factors that inhibit adpiogenesis 5. Experimental rationale Chapter II. cDNA cloning, expression and functional characterization of a novel 15-oxoprostaglandin-Δ13-reductase from 3T3-L1 adipocytes. ……………………14 1. Introduction 2. Materials and Methods 3. Results 4. Discussion 5. Figures and Legends Chapter III. Identification of 15-keto prostaglandin E2 as a PPAR-γ ligand. ……………………………………………38 1. Introduction 2. Materials and Methods 3. Results 4. Discussion 5. Figures and Legends Chapter IV. Modulation of PPAR-γ activation by PGE2 catabolism. ……………………………………………………55 1. Introduction 2. Materials and Methods 3. Results 4. Discussion 5. Figures and Legends References…………………………………………………………72 Appendix | |
| dc.language.iso | en | |
| dc.title | 前列腺素的分解代謝在脂肪細胞分化過程中所扮演的角色 | zh_TW |
| dc.title | The role of prostaglandin catabolism in adipocyte differentiation. | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 95-2 | |
| dc.description.degree | 博士 | |
| dc.contributor.oralexamcommittee | 莊立民,王惠鈞,林榮耀,陳青周 | |
| dc.subject.keyword | 前列腺素,脂肪細胞分化, | zh_TW |
| dc.subject.keyword | prostaglandin,PPAR-γ,adipocyte differentiation, | en |
| dc.relation.page | 83 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2007-07-19 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 生物化學暨分子生物學研究所 | zh_TW |
| 顯示於系所單位： | 生物化學暨分子生物學科研究所 | |
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