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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 呂紹俊(Shao-Chun Lu) | |
| dc.contributor.author | Huai-Tzu Li | en |
| dc.contributor.author | 黎懷慈 | zh_TW |
| dc.date.accessioned | 2021-05-17T09:16:34Z | - |
| dc.date.available | 2012-09-19 | |
| dc.date.available | 2021-05-17T09:16:34Z | - |
| dc.date.copyright | 2012-09-19 | |
| dc.date.issued | 2012 | |
| dc.date.submitted | 2012-07-31 | |
| dc.identifier.citation | 高品筠(2008) 顆粒性白血球群落刺激因子可刺激Akt/GSK3β/NFκB的訊息傳遞以抑制內毒素引起之過渡活化的微膠細胞。慈濟大學藥理暨毒理學研究所
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/6702 | - |
| dc.description.abstract | 顆粒性白血球群落刺激因子(G-CSF)為造血性醣蛋白家族中的一員，也是一種細胞激素，主要由巨噬細胞及單核球細胞所分泌，具有促進噬中性白血球分化、增生及移動的功能。細胞受到LPS刺激活化p38 MAPK會使G-CSF mRNA穩定度增加，增加G-CSF表現。G-CSF mRNA的穩定度主要由 3'UTR的ARE及SLDE所調控。許多研究顯示給予SB203580抑制p38 MAPK活性後，會使在3’UTR帶有ARE的mRNA半衰期變短，進而降低其表現量。但是本實驗室先前的研究結果發現，以小鼠巨噬細胞Raw264.7經LPS刺激之下預先給予SB203580，會增加G-CSF mRNA的穩定度，更增加LPS誘導的G-CSF mRNA及蛋白質的表現量，顯示SB203580對G-CSF表現的影響與對其他帶有ARE的細胞激素的mRNA作用是不同的。本研究的目的是探討SLDE在SB203580增
加LPS誘導的G-CSF mRNA穩定度所扮演的角色。 實驗結果發現當細胞不受刺激時G-CSF 3’UTR會使mRNA不穩定；而給予LPS及SB203580後會提高mRNA穩定度。將3’UTR接到luciferase後，以site direct mutagenesis分析發現SB203580提高LPS誘導的G-CSF mRNA穩定度是透過3’UTR SLDE內TTTAATATTTA這段高保留性序列。此外，不同的p38 MAPKs抑制劑對G-CSF mRNA及蛋白質的量有不同的影響，其中預先給予SB203580、SB202190及PD169316都會提高G-CSF mRNA穩定度進而提高LPS誘導的mRNA及蛋白質表現，而SKF86002及SB239063則不會影響G-CSF蛋白質表現，但是SKF86002也會些微增加約1.8倍的mRNA表現。最後我們也發現在沒有LPS刺激的情況下，SB203580、SB202190及PD169316也會透G-CSF 3’UTR來增加G-CSF mRNA穩定度，顯示這些抑制劑增加G-CSF mRNA穩定度可能不是藉由抑制p38 MAPKs磷酸酶活性所導致。綜合以上結果，SB203580會透過SLDE中高保留性的序列提高G-CSF mRNA穩定度，而且SB203580增加G-CSF mRNA的作用可能不是藉由抑制p38 MAPKs磷酸酶活性所導致。 | zh_TW |
| dc.description.abstract | Granulocyte colony stimulating factor (G-CSF) is not only a member of hematopoietic growth factor but also a cytokine. G-CSF is known to control the production, differentiation and migration of neutrophils. LPS increasing G-CSF mRNA stability by activating p38 MAPK kinase activity, thus increases G-CSF production. There are two destabilizing elements in G-CSF 3’UTR-adenosine uridine-rich element (ARE) and stem-loop destabilizing element (SLDE) that regulate G-CSF mRNA stability. Numerous studies show that SB203580, a pyridinyl imidazole p38 MAPK inhibitors, reduces the half-life of the ARE-containing mRNA by inhibiting p38 MAPK kinase activity. However, our previous studies showed that SB203580 enhances LPS-induced G-CSF production by increasing mRNA stability. The aim of this study is to investigate the possible role of SLDE in SB203580 mediated increase in G-CSF mRNA stability in LPS treated macrophage.
Our results show that G-CSF 3’UTR decreases mRNA stability in unstimulated cells, but stabilized mRNA when p38 MAPKs activity was activated by LPS. We find that the consensus sequence “TTTAATATTTA” rather than the stem-loop structure in G-CSF 3’UTR SLDE is essential for the SB230580 enhanced LPS-increased G-CSF mRNA stability. Moreover, various p38 MAPK inhibitors had different effects on the expression levels of G-CSF mRNA and protein. The levels of LPS-induced G-CSF mRNA and protein in Raw 264.7 were increased by SB203580, SB202190 and PD169316, but not by SB239063. Furthermore, we discovered that SB203580, SB202190 and PD169316 increased G-CSF mRNA stability when p38 MAPK kinase activity was inactivated. Taken together, these results suggest that SB203580 increases G-CSF mRNA stability through the highly conserved sequence and this effect is independent p38 MAPKs kinase inhibition. | en |
| dc.description.provenance | Made available in DSpace on 2021-05-17T09:16:34Z (GMT). No. of bitstreams: 1 ntu-101-R99442011-1.pdf: 3509540 bytes, checksum: 0bf8dd944970c305ec485d0e2952b389 (MD5) Previous issue date: 2012 | en |
| dc.description.tableofcontents | 口試委員審定書........................................ i
謝誌.................................................. ii 摘要.................................................. viii 第一章 緒論........................................... 1 第一節 文獻回顧....................................... 2 第二節 研究動機及目的................................. 16 第二章 材料方法....................................... 17 實驗材料.............................................. 18 第二節 細胞培養....................................... 19 第三節 細胞毒殺活性測試之檢測......................... 20 第四節 細胞內RNA抽取與基因表現量分析 ..................21 第五節 蛋白質表現量分析............................... 24 第六節 質體的建構. .....................................28 第七節 螢火蟲冷光酶活性分析 (luciferase activity assay)................................................ 34 第八節 資料統計分析................................... 36 第三章 實驗結果....................................... 37 第一節 探討SB203580增加LPS誘導的G-CSF mRNA穩定度是否是透過 G-CSF mRNA 3’UTR..................................... 38 第二節 探討SB203580增加LPS誘導的G-CSF mRNA穩定度是透過G-CSFmRNA 3’UTR當中哪一段序列.......................... 39 第三節 探討不同p38 MAPK抑制劑對LPS誘導的G-CSF mRNA表現的影響................................................... 41 第四節 探討只單獨處理SB203580是否就會增加G-CSF mRNA表現................................................... 43 第四章 討論.......................................... 45 第一節SB203580透過G-CSF mRNA 3'UTR SLDE來增加LPS誘導的G-CSF mRNA穩定度........................................... 46 第二節 LPS除了透過ARE之外也會透過SLDE增加G-CSF mRNA穩定度................................................... 47 第三節 不同p38MAPKs抑制劑對LPS誘導的G-CSF mRNA表現有不同影響................................................... 48 第四節 單獨處理SB203580、SB202190和PD169316增加G-CSF mRNA穩定度不是藉由抑制p38 MAPKs磷酸酶活性所導致............ 50 第五節 結論.......................................... 52 第五章 圖表.......................................... 53 參考文獻............................................. 70 附錄................................................. 85 | |
| dc.language.iso | zh-TW | |
| dc.title | 位於G-CSF 3'端UTR之SLDE序列在SB203580誘導下增加G-CSF mTNA穩定度的角色 | zh_TW |
| dc.title | Role of SLDE in G-CSF 3'UTR mediates increase of mRNA stability induced by SB203580 | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 100-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 張淑芬,繆希椿,余明俊 | |
| dc.subject.keyword | 顆粒性白血球刺激因子,SB203580,stem-loop destabilizing element (SLDE),mRNA穩定度,p38 MAPK, | zh_TW |
| dc.subject.keyword | G-CSF,SB203580,SLDE,mRNA stability,p38 MAPK, | en |
| dc.relation.page | 95 | |
| dc.rights.note | 同意授權(全球公開) | |
| dc.date.accepted | 2012-08-01 | |
| 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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