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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
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dc.contributor.advisor | 鄭景暉(Jiiang-Huei Jeng) | |
dc.contributor.author | Yen-Chen Wang | en |
dc.contributor.author | 王彥臻 | zh_TW |
dc.date.accessioned | 2021-06-16T10:31:46Z | - |
dc.date.available | 2013-09-24 | |
dc.date.copyright | 2013-09-24 | |
dc.date.issued | 2013 | |
dc.date.submitted | 2013-08-14 | |
dc.identifier.citation | Abramovitz M, Rodan G, Harada S (2001). Expression of the prostaglandin E2 (PGE2) receptor subtype EP4 and its regulation by PGE2 in osteoblastic cell lines and adult rat bone tissue. Bone 28:275-281.
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Arch Oral Biol. 16:1143-54 Camargo P, Lagos R, Pirih F, Benitez A, Nervina J, Tetradis S (2005). Prostaglandins E2 and F2α enhance differentiation of cementoblastic cells. J Periodontol 76:303-09. Zhang X, Schwarz EM, Young DA, Puzas JE, Rosier RN, O’Keefe RJ (2002). Cyclooxygenase-2 regulates mesenchymal cell differentiation into the osteoblast lineage and is critically involved in bone repair. J Clin Invest . 109:1405-15. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/60823 | - |
dc.description.abstract | 實驗目的: 在牙髓受感染或發炎的過程中,前列腺素E2是重要因子來調節牙髓細胞的生理病理功能。本篇論文目的在探討前列腺素E2對人類牙髓細胞的調節作用、相關EP receptor被活化後的角色扮演及訊息傳導。
實驗方法: 本研究以前列腺素E2以及不同前列腺素E受體的促效劑(agonist)或是預先加入AC/PKA抑制劑三十分鐘後再給予前列腺素E2,來刺激培養的人類牙髓細胞,並觀察其細胞反應暨其訊息傳導路徑。 實驗結果: 1.前列腺素E2在我們所分析的濃度對牙髓細胞來說是抑制作用,且濃度越高抑制作用越明顯,此現象在cell migration及collagen turnover assay和鹼性磷酸酶染色都能觀察到。 2.加入EP2 agonist 19R-OH PGE2能影響人類牙髓細胞膠原蛋白之代謝,cell migration能力,以及鹼性磷酸酶的表現。 3.分別給予PKA抑制劑H89(濃度1μM)以及腺苷酸環化酶ACs抑制劑SQ22536似乎能部分逆轉原先前列腺素E2抑制cell migration的情形及抑制鹼性磷酸酶的表現情形。 4.AP-1 轉錄因子表現上升與改變,證實AP-1在前列腺素E2調控發炎反應扮演某種角色。 結論: 不論在ALP activity或者是cell migration的結果都可以指出前列腺素E2調節人類牙髓細胞這些作用主要以EP2受器為主,可能是藉由AC/PKA的路徑來調控。AP-1 轉錄因子表現上升改變,證實AP-1在前列腺素E2調控發炎反應扮演相當之角色。 | zh_TW |
dc.description.abstract | Aim: Bacterial infection and mechanical injuries can cause pulp inflammation. Prostanoids production of pulp cells were involved in the inflammatory and healing processes of dental pulp. These contradictory actions of PGE2 further support the presence of diverse PGE2 receptor isoforms in different tissues or cells. However, the significance of EP receptors in human dental pulp has not yet been fully described. The aim of the study is to investigate the role of EP receptors and their signaling in regulation of the dental pulp.
Materials and Methods: Primary-cultured human dental pulp cells were treated with PGE2 or EP receptor agonist. In some experiments, cells were pretreated with H89 (a PKA inhibitor), or SQ22536 (an ACs inhibitor) 30 minutes before adding PGE2. Cell migration assay has been used to examine signaling events. Collagen content was determined by Sircol Collagen assay. Cell differentiation and mineralization was evaluated by alkaline phosphatase (ALP) staining. Changes in mRNA expression were determined by reverse-transcriptase polymerase chain reaction (RT-PCR). Result:Cell under the treatment of PGE2 (0.1μM~10μM) showed a decrease of collagen formation and cell migration and also showed a decrease of ALP activity. CAY10598 (EP2 agonist) at low dose (0.5μM , 1μM) increased ALP activity. 19R-OH PGE2 (EP2 agonist) showed a decrease in cell migration assay and collagen formation assay . Pretreatment by H89 (a PKA inhibitor), or SQ22536 (an ACs inhibitor) were effective to reverse the inhibitory effect of PGE2 in ALP stain and in the cell migration assay. PGE2 can induce the expression of AP-1 transcription factors. Conclusion: Signal transduction of PGE2 in human dental pulp cell is complex, AC/PKA may take part in this complex system via EP2. PGE2 may be involved in dental pulp inflammation and repair processes via induction of AP-1 transcription factors. | en |
dc.description.provenance | Made available in DSpace on 2021-06-16T10:31:46Z (GMT). No. of bitstreams: 1 ntu-102-R99422005-1.pdf: 4298542 bytes, checksum: 56ebd3074eb7afc44aa48ac0e2f59f63 (MD5) Previous issue date: 2013 | en |
dc.description.tableofcontents | 謝致 II
中文摘要 III Abstract IV 第一章 前言 1 第二章、 文獻回顧 2 2.1 前列腺素的合成(Biosynthesis of Prostaglandins,PGs) 2 2.2 前列腺素E2的受器(Receptors of PGs) 3 2.3 ACs / PKA 訊息傳導路徑 3 2.4 前列腺素E2的訊息傳導路徑 5 2.5前列腺素E2於發炎反應中的角色扮演(Role of PGE2 in inflammation) 6 2.6牙髓牙本質複合體的修復機制(Reparative mechanism of pulpal-dentin complex) 7 2.7牙髓與牙本質修復之生物標記(Marker of pulpal repair & dentinogenesis) 8 第三章 研究假說和實驗目的 11 第四章 材料和方法 12 4.1實驗材料: 12 4.2 培養人類牙髓細胞: 12 4.3藥物對人類牙髓細胞的影響 13 4.4鹼性磷酸酶染色 13 4.5反轉錄聚合酶連鎖反應(Reverse Transcription Polymerse Chain Reaction (RT-PCR) 14 4.6膠原蛋白濃度的分析(Collagen Content Assay) 17 4.7 細胞遷移分析Cell migration assay /細胞劃痕法(scratch assay) 18 4.8 統計分析 20 第五章 結果 21 5.1人類牙髓細胞的型態觀察 21 5.2細胞遷移實驗(Cell Migration Assay ) 21 5.3膠原蛋白濃度的測定(Assay of Collagen Turnover) 23 5.4鹼性磷酸酶活性測試(ALP staining) 24 5.5聚合酶連鎖反應PCR: PGE2對AP-1 轉錄因子的影響 25 第六章 討論 26 6.1前列腺素E2的受器(Receptors of PGE2) 26 6.3細胞的培養 28 6.4前列腺素E2與細胞分化 29 6.5訊息傳導路徑 30 6.6細胞遷移實驗 (Cell Migration Assay) 32 第七章 結論 34 參考資料 36 | |
dc.language.iso | zh-TW | |
dc.title | 前列腺素E2對人類牙髓細胞的調節作用:EP receptor被活化後的角色扮演及訊息傳導 | zh_TW |
dc.title | Regulation of PGE2 on the Human Dental Pulp Cells : Role of EP Receptors Activation and Their Signaling | en |
dc.type | Thesis | |
dc.date.schoolyear | 101-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 張美姬,張國威,張育超,林俊彬 | |
dc.subject.keyword | 牙髓細胞,PGE2,前列腺素受體,膠原蛋白,鹼性磷酸?AP-1 轉錄因子,訊息傳導, | zh_TW |
dc.subject.keyword | dental pulp cells,PGE2,collagen,alkaline phosphatase,AP-1 transcription factors,prostaglandin receptor, | en |
dc.relation.page | 76 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2013-08-14 | |
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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