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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 呂紹俊(Shao-Chun Lu) | |
| dc.contributor.author | Yu-Pei Huang | en |
| dc.contributor.author | 黃昱裴 | zh_TW |
| dc.date.accessioned | 2021-06-16T13:04:24Z | - |
| dc.date.available | 2015-09-24 | |
| dc.date.copyright | 2013-09-24 | |
| dc.date.issued | 2013 | |
| dc.date.submitted | 2013-08-05 | |
| dc.identifier.citation | 蔡雯茹 (2010). SB203580增加G-CSF mRNA 的穩定度進而增加巨噬細胞中LPS誘發G-CSF的產生。國立台灣大學醫學院生物化學暨分子生物學研究所碩士論文
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/61501 | - |
| dc.description.abstract | 顆粒性白血球群落刺激因子 (Granulocyte colony-stimulating factor, G-CSF)是造血性醣蛋白生長因子的成員之一，具有促進白血球增生、分化、成熟及移動的功能。主要由巨噬細胞、內皮細胞所分泌，當LPS、IL-1β 或TNF-α 刺激時，透過轉錄及後轉錄增加 G-CSF 表現。G-CSF mRNA 穩定度主要由三端非轉譯區 (3’ untranslated region, 3’UTR) 的 ARE (AU-rich element) 及 SLDE (stem-loop destabilizing element)所調控。多篇文獻報導在 p38 MAPK 訊息路徑活化下，給予
SB203580 會降低 3’UTR 帶有 ARE 細胞激素的表現。然而，實驗室先前的研究結果發現，在有或沒有LPS刺激下，於RAW264.7細胞中給予SB203580可透過3’UTR的SLDE序列穩定G-CSF mRNA進而增加其表現。顯示 SB203580 增加G-CSF表現可能不是透過p38α/β MAPK所導致的。本研究目的首先要確認 SLDE 及p38α/β MAPK 在 SB203580 增加 G-CSF mRNA 穩定度的作用中扮演的角色；接著用microarray 分析探討是否有其他基因也會受到 SB203580 所誘導，並分析這些被誘導的基因其 3’UTR 是否帶有類似 SLDE 的序列。最後探討目前已知與發炎反應相關的miRNA是否參與 SB203580 增加G-CSF mRNA 穩定度的作用。以site-direct mutagenesis 改變SLDE的序列發現 SB203580 是透過 SLDE序列穩定G-CSF mRNA ，與莖-環結構較無關。將RAW264.7細胞中p38α或p38β MAPK knockdown後發現雖然 LPS 誘導的G-CSF 表現會受到p38α MAPK knockdown 的影響而下降，然而，在有或沒有 LPS 刺激下，SB203580 可在p38α 或p38β MAPK knockdown 細胞增加 G-CSF mRNA 穩定度及蛋白質表現。Microarray實驗結果找到在有或沒有 LPS 刺激下 SB203580 都能增加其表現量共 21個基因，其中 Gnpda1 3’UTR也帶有類似 SLDE 序列。最後利用miRNA PCR array實驗發現目前已知與發炎反應調節相關的 miRNA中有 7個會受 SB203580 所調節，由 miRWalk 預測軟體分析發現G-CSF 3’UTR 中並沒有這 7個 miRNA的結合位子，顯示 SB203580 可能不是透過這 7 個 miRNA 直接調控 G-CSF 的表現，但我們也不能完全排除這些miRNA間接調控的可能。綜合以上實驗結果，SB203580透過G-CSF 3’UTR的SLDE序列穩定mRNA進而增加其表現的作用機制與 p38α/β MAPK無關，可能是透過其他機制來調節。 | zh_TW |
| dc.description.abstract | Granulocyte-colony stimulating factor (G-CSF) is a member of the glycoprotein growth factor family that regulates granulocyte production, neutrophil maturation and mobilization. The main sources of G-CSF are fibroblast cells, endothelial cells and macrophages. The production of G-CSF is induced by inflammatory stimuli, such as LPS, TNF-α and IL-1β. The expression of G-CSF is regulated at both transcriptional
and posttranscriptional levels. In the 3’-UTR of G-CSF mRNA, there are two destabilizing elements, AU-rich elements (ARE) and stem-loop destabilizing element (SLDE), these elements have been identified conserved among different species. Our previous results showed that SB203580, a pyridinyl imidazole inhibitor of p38α/β MAPK, enhances G-CSF production by increasing mRNA stability in the presence or absence of LPS. Moreover, the sequence of SLDE in G-CSF 3’UTR is identified essential for SB203580-induced increase of mRNA using a luciferase-G-CSF 3’UTR reporter system. In this study, our first aim is to further confirm the role of SLDE in SB203580-induced increase of G-CSF mRNA stability; and to investigate the involvement of p38α/β MAPK in SB203580-induced G-CSF expression. Second aim is to determine if SB203580 can up-regulate other transcripts and if 3’-UTR of these transcripts also contain SLDE sequence. Third aim is to explore whether miRNA involves in SB203580-induced G-CSF expression. Using site-direct mutagenesis mutated one or two bases on SLDE, we further confirmed that SLDE in G-CSF 3’UTR is critical for SB203580-induced increase of G-CSF mRNA. The p38α and p38β MAPK were knockdown separately in RAW264.7 by infected with lentivirus carrying specific shRNA. We found that SB203580 induces increase of G-CSF mRNA in p38α or p38β knockdown cells in the presence or absence of LPS. The results indicate that SB203580-induced increase of G-CSF expression is independent of p38α or p38β MAPK. In microarray analysis, 21 genes were identified to be up-regulated by SB203580 in the presence or absence of LPS. Only one of 21 genes, Gnpda1, contains a SLDE-like sequence in the 3’UTR. Moreover, we investigate the involvement of inflammatory-related miRNAs in this mechanism by miRNA PCR array. Seven miRNAs were found to be regulated by SB203580, but 3’UTR of G-CSF does not contain binding site for these miRNAs. The results indicate that these inflammatory-related miRNA may not directly involve in SB203580-induced increase of G-CSF expression. But the indirect involvements of these miRNAs cannot be exclude. Taken together, our data show that SB203580 increases both G-CSF mRNA and protein levels by stabilizing G-CSF mRNA through the conserved SLDE sequence in the 3’UTR; however, the effect is independent of p38α/β MAPK. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-16T13:04:24Z (GMT). No. of bitstreams: 1 ntu-102-R00442017-1.pdf: 4042321 bytes, checksum: 034b10458b3fd3e40a4c33e519078bf3 (MD5) Previous issue date: 2013 | en |
| dc.description.tableofcontents | 口試委員審定書 I
謝誌 II 摘要 VIII Abstract X 第一章 緒論 1 第一節 文獻回顧 2 第二節 研究動機及目的 20 第二章、材料與方法 22 第一節 實驗材料 23 第二節 細胞培養 24 第三節 細胞內RNA抽取與基因表現量分析 25 第四節 製備慢病毒 (lentivirus)與慢病毒的感染 (Infection) 28 第五節、蛋白質表現量分析 32 第六節 質體的建構 36 第七節 螢火蟲冷光酶活性分析 (Luciferase reporter assay) 39 第八節 微陣列分析 (microarray) 41 第九節 miScript miRNA PCR Array 42 第十節 資料統計分析 43 第三章 實驗結果 44 第一節 進一步探討SB203580是否透過G-CSF 3’UTR中SLDE序列增加其mRNA 穩定度 45 第二節 探討p38α 及p38β MAPK是否參與LPS所誘導G-CSF mRNA表現的作用機制 46 第三節 探討p38α 及p38β MAPK是否參與SB203580更增加LPS所誘導的G-CSF mRNA表現的作用機制 47 第四節 探討單獨給予SB203580的情況下p38α 及p38β MAPK是否參與增加G-CSF表現的作用機制 48 第五節 利用mouse microarray分析探討是否有其他mRNA也會受到SB203580誘導增加其表現 49 第六節 利用miRNA PCR Array探討是否有miRNA參與SB203580增加G-CSF mRNA表現的作用機制 51 第四章 討論 53 第一節 SB203580透過G-CSF 3’UTR的SLDE增加G-CSF mRNA穩定度 54 第二節 p38α/β MAPK在LPS誘導產生G-CSF過程中扮演的角色 55 第三節 給予LPS刺激的p38α/β MAPK knockdown細胞中，SB203580對不同細胞激素的調節 56 第四節 在p38α/β MAPK knockdown細胞中單獨給予SB203580對不同細胞激素的調節 57 第五節 由mouse microarray分析所篩選出SB203580所誘導表現的目標基因 59 第六節 miRNAs與RNA-binding proteins在此作用機制中可能扮演的角色 61 第七節 結論 63 第五章 圖表 65 補充 83 附錄 86 參考文獻 101 | |
| dc.language.iso | zh-TW | |
| dc.subject | p38α/β MAPK | zh_TW |
| dc.subject | miRNA | zh_TW |
| dc.subject | 顆粒性白血球群落刺激因子 | zh_TW |
| dc.subject | SLDE (stem-loop destabilizing element) | zh_TW |
| dc.subject | SB203580 | zh_TW |
| dc.subject | stem-loop destabilizing element(SLDE) | en |
| dc.subject | p38α/β MAPK | en |
| dc.subject | miRNA | en |
| dc.subject | G-CSF | en |
| dc.subject | SB203580 | en |
| dc.title | p38α/β MAPK在SB203580誘導下增加RAW264.7細胞中G-CSF表現的角色 | zh_TW |
| dc.title | Roles of p38α/β MAPK in SB203580-induced G-CSF expression in RAW264.7 | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 101-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 張淑芬(Shwu-Fen Chang),姜安娜(An-Na Chiang),張博淵(PO-YUAN CHANG) | |
| dc.subject.keyword | 顆粒性白血球群落刺激因子,p38α/β MAPK,SB203580,SLDE (stem-loop destabilizing element),miRNA, | zh_TW |
| dc.subject.keyword | G-CSF,p38α/β MAPK,SB203580,stem-loop destabilizing element(SLDE),miRNA, | en |
| dc.relation.page | 114 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2013-08-05 | |
| 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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