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探討成體細胞核重編程的機制與其在人類角膜內皮細胞的應用潛力

為了解決PX COOK ptt的問題，作者林柏穎 這樣論述：

目錄指導教授推薦書口試委員審定書誌謝 iiiAbstract iv中文摘要 vi目錄 viiiList of figures xiiList of appendixes xivRational and Specific aims xvChapter 1 Background 11.1 Cell potency 11.2 Embryonic stem cells 31.3 Induced pluripotent stem cells 41.4 Applications of iPSCs 51.5 The reprogram

process 61.6 Elite and stochastic model 71.7 Mesenchymal-to-epithelial transition 81.8 The role of E-cadherin 91.9 Human corneal endothelial cells 9Chapter 2 Materials and methods 112.1 Mouse husbandry and genotyping 112.2 Cell culture 112.3 Electroporation 122.4 Quantita

tive RT PCR 122.5 iPSC generation 122.6 Immunostaining 132.7 Western blotting 132.8 ELISA and soft agar assay for quantitation of functional LIF 142.9 TGF releasing assay 152.10 Lentivirus production 152.11 Teratoma formation and chimeric mouse generation 162.12 Flat mount

172.13 Penetrating keratoplasty 17Chapter 3 Results 183.1 Establishment of the Col1a1 4F2A-Oct4-GFP mouse 183.2 MEFCol1a1 4F2A-Oct4-GFP respond to doxycycline induction and alteration of cell fate 193.3 MEFCol1a1 4F2A-Oct4-GFP are able to generate iPSCs in chemically defined medium

203.4 Different culture media affect the proliferation of MEFCol1a1 4F2A-Oct4-GFP in vitro 223.5 High efficiency of iPSC generation does not depend on the ability of the culture medium to support the initial rapid proliferation of MEFCol1a1 4F2A-Oct4-GFP 233.6 Distinct processes of iPSC genera

tion observed under different culture conditions 253.7 Initial MEF seeding density and feeder adoption affect iPSC generation 273.8 TGF-beta secreted from feeder cells impedes iPSC generation 283.9 iPSCCol1a1 4F2A-Oct4-GFP displays pluripotency markers, forms teratoma in NOD-SCID mice, and

possesses germline transmission capacity 313.10 Engineered feeders raise the reprogramming efficiency 333.11 E-cadherin-engineered feeders do improve the reprogramming efficiency 343.12 The interaction between E- and N-cadherin in the early stage of somatic reprogramming promotes the phosph

orylation of Stat3 353.13 Polarity serves as a critical feature in functional HCECs 373.14 The distribution pattern of ZO-1 is shifted when cells are plated on gelatin- or vitronectin-coated dish 383.15 The distribution pattern of ZO-1 in the induced HCECs significantly located in the apica

l region of the cell 39Chapter 4 Discussion 404.1 Adopting the microenvironment helps Col1a1 4F2A-Oct4-GFP mouse to provide a homogenous platform to generate iPSCs 404.2 The microenvironment is involved in driving route choice 424.3 The interaction between E-cadherin and N-cadherin gover

ns the early stage of reprogramming 454.4 Matrix manipulating improves the polarity of induced HCECs 46References 48Figures 74Appendixes 96List of figuresFigure 1: Breeding strategy and genotyping of the Col1a1 4F2A-Oct4-GFP mouse. 74Figure 2: MEFCol1a1 4F2A-Oct4-GFP respond to dox

ycycline induction for cell fate alteration. 75Figure 3: Almost every MEFCol1a1 4F2A-Oct4-GFP expresses the OSKM cassette after doxycycline induction. 76Figure 4: MEFCol1a1 4F2A-Oct4-GFP are able to generate iPSCs in various media with different efficiencies. 77Figure 5: High efficiency of

iPSC generation does not depend on the ability of the culture medium to support the rapid proliferation of MEFCol1a1 4F2A-Oct4-GFP. 78Figure 6: MEFCol1a1 4F2A-Oct4-GFP seeding density and feeder cells affect the iPSC generation rate. 80Figure 7: Feeder cells secrete TGF-beta impeding iPSC gene

ration likely via the process of mesenchymal-epithelial transition. 81Figure 8: iPSCs derived from MEFCol1a1 4F2A-Oct4-GFP exhibit pluripotency as seen in mouse ESCs. 84Figure 9: The iPSCCol1a1 4F2A-Oct4-GFP is competent at germline transmission. 86Figure 10: Various improvement of reprogra

mming efficiency in different engineered SNLs. 87Figure 11: The reprogramming efficiency is increased while culturing on E-cadherin-engineered SNL. 88Figure 12: E-cadherin interacts with N-cadherin and promote the phosphorylation of STAT3 in reprogramming improvement. 89Figure 13: Human cor

neal endothelial cells induced from iPSCs are not in function. 92Figure 14: Identifying the polarity improvement through different matrixes in vitro. 94Figure 15: The polarity of Human corneal endothelial cells induced from iPSCs is improved while culturing on gelatin or vitronectin. 95List

of appendixesFigure 1: The construct map for SNL engineering. 96Table 1. Genotyping primer sets for each transgene. 100Table 2. The temperature setting for Genotyping. 101Table 3: Recipe for the media (MEF, iSF, iCD, VC6TFNZ, R1 ESC media). 103Table 4: The primer sets used in real-time

PCR. 104

探討巨噬細胞促發炎與非發炎beta-葡聚醣處理後之對巨噬細胞典型與另類活化的影響

為了解決PX COOK ptt的問題，作者徐泱彤 這樣論述：

前言：Beta-glucans，以beta醣苷鍵鍵結的葡萄糖聚合體，廣泛分布於自然界，並發現存在於細菌、真菌、蕈類、藻類或高等植物等細胞壁中。現今，已得知beta-glucans具有許多免疫刺激的功能，以beta-(1,3)-glucan及beta-(1,3)(1,6)-glucan的研究最為廣泛，其具有提高抵抗細菌、真菌的能力或抗癌的效果等；beta-(1,3)(1,4)-glucan則有降低心血管疾病發生，直至近期才有免疫相關的研究。在實驗室先前的實驗中發現植物來源為主的beta-(1,3)(1,4)-glucan不具刺激巨噬細胞發炎反應，並提高scavenger receptors表現

，刺激巨噬細胞Lys M與Arg-1基因表達，此現象與M2另類巨噬細胞活化表現相類似，後歸類為「非發炎型beta-glucans」。相反地，微生物來源為主的beta-(1,3)-glucan及beta-(1,3)(1,6)-glucan活化巨噬細胞NO與TNF-的分泌，並降低Arg-1與Lys M基因表達，此現象與M1典型巨噬細胞活化表現相似，後歸類稱為「促發炎型beta-glucans」。本篇目的為延續性試驗，分類市售六種且不同來源的高純度beta-glucans為非發炎型beta-glucans或促發炎型beta-glcuans，並以共同活化巨噬細胞方式，以探討兩類beta-glucan

s間對於不同巨噬細胞之典型或另類途徑活化作用之影響，以進一步瞭解不同來源beta-glucan在巨噬細胞功能與結構上的關係。材料與方法：六種市售不同來源、高純度的非發炎型beta-glucans來自於昆布 (Laminaria digitata, laminarin, LA)大麥 (barley, GB)與地衣 (lichenan, LI)和促發炎型beta-glucans來自於真菌 (Saccharomyces cerevisiae, zymosan, ZY)、眼蟲 (Euglena gracilis, paramylon, EG)及細菌 (Alcaligenes faecalis, cur

dlan, CD)與三種不同的巨噬細胞 (RAW264.7、J77A.1與小鼠腹腔巨噬細胞)進行非發炎型與發炎型beta-glucans共同培養，測量NO產生、oxidative burst、lysozyme activity，甚至是iNOS、Lys M、arg-1 mRNA的表達，另外亦測定了TNF-與IL-10細胞激素的表現量。結果與討論：受ZY與CD刺激活化的RAW264.7巨噬細胞細胞株與小鼠腹腔巨噬細胞與非發炎型beta-glucans共同培養產生大量促發炎因子及IL-10，此因可能是巨噬細胞具有強烈發炎反應，而使IL-10分泌。受EG刺激活化的RAW264.7巨噬細胞細胞株與小鼠

腹腔巨噬細胞與非發炎型beta-glucans共同培養產生比其他兩種促發炎型beta-glucans活化之巨噬細胞產生的發炎反應較輕微，但同時產生IL-10調控發炎反應。另外，促發炎型beta-glucans無法將J774A.1巨噬細胞細胞株極化成M1典型巨噬細胞。