DSPE-PEG-PDP调控金表面脂质体破裂行为及tLBM形成机制研究
DSPE-PEG-PDP改善金外表面脂质体碎裂举动及tLBM出现管理机制探索链接搜索://pubs.acs.org/doi/abs/10.1021/la300127m做者:王曦马修·M·辛德尔王思文雷吉娜·拉根*英文论文:在水性聚氨酯储存液标准下,灵活运用共价键力光学显微镜 (AFM) 深入分析了脂质体(由特大型编织成单层囊泡組成)与基低外观中间的无机化学人格魅力,科学探究其在金外观推动囊泡分裂和绳束脂质双层线路膜 (tLBM) 成型的功用。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) 增长到 1-棕榈酰-2-油酰-sn-甘油-3-磷酸胆碱 (POPC) 囊泡中,以推进完成金-硫醇盐键成型的间接功用。在有侵入性和法压和无侵入性和法压标准下,AFM 检测器检测器诱惑的引致金外观囊泡分裂的力被程序化为 DSPE-PEG-PDP 多组分的数学函数。所致包含的 2.5、5 和 10 mol % DSPE-PEG-PDP 的囊泡分裂所用要的的临界状态状态力不同约为 1.1、0.8 和 0.5 nN。就包含的 2.5 mol % DSPE-PEG-PDP 的囊泡,tLBM 成型所用要的的临界状态状态力从 1.1 nN(无侵入性和法压)降低 0.6 nN(5 mM CaCl 2所致的侵入性和法压)。高达到 5 nN 的力不会引致纯 POPC 囊泡在金上成型 LBM。DSPE-PEG-PDP 或许就在金外观锚定和变行囊泡是非常重要的要。一项深入分析展出了怎么才能灵活运用功能模块性脂质来调低囊泡-外观间接功用,并指出了囊泡-底物间接功用在囊泡分裂中的功用。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.