DSPE-PEG-PDP自我调节金外壁脂质体断裂习惯及tLBM构成系统探索微信链接：//pubs.acs.org/doi/abs/10.1021/la300127m作著：王曦马修·M·辛德尔王思文雷吉娜·拉根*论文摘要：在水性聚氨酯缓冲器液状况下，灵活运用分子力光学显微镜 (AFM) 分析了脂质体（由中小型双层线路囊泡组合）与基低表明间接之间的化学上的人格魅力，实验设计其在金表明驱使囊泡受损和束博脂质双层线路膜 (tLBM) 构成的功用。将 1,2-二硬脂酰-sn-甘油-3-磷酸酒精胺-N-聚乙二醇-2000 -N- [3-(2-吡啶基二硫代)丙酸酯] (DSPE-PEG-PDP) 修改到 1-棕榈酰-2-油酰-sn-甘油-3-磷酸胆碱 (POPC) 囊泡中，以增进按照金-硫醇盐键构成的间接功用。在有进行浸入到工作会更压和无进行浸入到工作会更压状况下，AFM 测试检测器测试检测器诱导性的会造成金表明囊泡受损的力被批量为 DSPE-PEG-PDP 酚类化合物的变量。引发内含 2.5、5 和 10 mol % DSPE-PEG-PDP 的囊泡受损流程的临介状态力对应约为 1.1、0.8 和 0.5 nN。来说内含 2.5 mol % DSPE-PEG-PDP 的囊泡，tLBM 构成流程的临介状态力从 1.1 nN（无进行浸入到工作会更压）下降 0.6 nN（5 mM CaCl 2引发的进行浸入到工作会更压）。高达独角兽 5 nN 的力就说会造成纯 POPC 囊泡在金上构成 LBM。DSPE-PEG-PDP 仍然来说在金表明锚定和和变形囊泡非常重要要。这个分析展示出了该怎样灵活运用的反应性脂质来可以调节囊泡-表明间接功用，并展现了囊泡-底物间接功用在囊泡受损中的功用。AbstractAtomic force microscopy (AFM) studies under aqueous buffer probed the role of chemical affinity between liposomes, consisting of large unilamellar vesicles, and substrate surfaces in driving vesicle rupture and tethered lipid bilayer membrane (tLBM) formation on Au surfaces. 1,2-Distearoyl-sn-glycero-3-phosphoethanolamine-N-poly(ethylene glycol)-2000-N-[3-(2-pyridyldithio) propionate] (DSPE-PEG-PDP) was added to 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) vesicles to promote interactions via Au–thiolate bond formation. Forces induced by an AFM tip leading to vesicle rupture on Au were quantified as a function of DSPE-PEG-PDP composition with and without osmotic pressure. The critical forces needed to initiate rupture of vesicles with 2.5, 5, and 10 mol % DSPE-PEG-PDP are approximately 1.1, 0.8, and 0.5 nN, respectively. The critical force needed for tLBM formation decreases from 1.1 nN (without osmotic pressure) to 0.6 nN (with an osmotic pressure due to 5 mM of CaCl2) for vesicles having 2.5 mol % DSPE-PEG-PDP. Forces as high as 5 nN did not lead to LBM formation from pure POPC vesicles on Au. DSPE-PEG-PDP appears to be important to anchor and deform vesicles on Au surfaces. This study demonstrates how functional lipids can be used to tune vesicle–surface interactions and elucidates the role of vesicle–substrate interactions in vesicle rupture.

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