Binding of Lipopolysaccharide and Cholesterol-Modified Gelatin on Supported Lipid Bilayers: Effect of Bilayer Area Confinement and Bilayer Edge Tension
Binding of Lipopolysaccharide and Cholesterol-Modified Gelatin on Supported Lipid Bilayers: Effect of Bilayer Area Confinement and Bilayer Edge Tension
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脂多糖和胆固醇改性明胶在支撑脂质双层上的结合：双层区域限制和双层边缘张力的影响
DOI：
10.1021/acs.langmuir.5b04302
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发表时间：
2016
期刊：
影响因子：
3.9
通讯作者：
T.
中科院分区：
文献类型：
--
作者：
Kataoka-Hamai;C.; Kaizuka;Y.; Taguchi;T.
两亲分子与支持的脂质双分子层（slb）的结合通常导致脂质原纤维从slb延伸。先前的研究表明，具有大而灵活的亲水区域的两亲分子通过其亲水区域诱导膜弯曲，从而触发slb中脂质纤维的形成。然而，尚无实验研究证实这种纤维形成机制。在这项工作中，我们使用荧光显微镜研究了脂多糖（LPS）和胆固醇修饰明胶与slb的结合。采用限制和不限制双分子层面积的slb来确定原纤维产生的机制。我们发现脂质纤维形成的主要原因是双分子层面积约20%的扩张，而不是膜曲率的增加。这些数据表明，即使结合的两亲分子具有较大的亲水结构域，双分子层面积约束在slb的形态变化中也起着关键作用。我们还发现，LPS插入后双层面积的变化取决于SLB的斑块形状。当SLB贴片由宽的双分子层段与长而薄的条纹相连时，双分子层面积的扩展主要发生在双分子层条纹内。结果表明，LPS的插入导致净脂质从宽双分子层区域流向条纹区域。面积的差异增加可以用平面双层条纹的不稳定性来解释，这种不稳定性源于沿双层边缘产生的线张力的大能量贡献。
Binding of amphiphilic molecules to supported lipid bilayers (SLBs) often results in lipid fibril extension from the SLBs. Previous studies proposed that amphiphiles with large and flexible hydrophilic regions trigger lipid fibril formation in SLBs by inducing membrane curvature via their hydrophilic regions. However, no experimental studies have verified this mechanism of fibril formation. In this work, we investigated the binding of lipopolysaccharide (LPS) and cholesterol-modified gelatin to SLBs using fluorescence microscopy. SLBs with restricted and unrestricted bilayer areas were employed to identify the mechanism of fibril generation. We show that the main cause of lipid fibril formation is an approximately 20% expansion in the bilayer area rather than increased membrane curvature. The data indicate that bilayer area confinement plays a critical role in morphological changes of SLBs even when bound amphiphilic molecules have a large hydrophilic domain. We also show that bilayer area change after LPS insertion is dependent on the patch shape of the SLB. When an SLB patch consists of a broad bilayer segment connected to a long thin streak, bilayer area expansion mainly occurs within the bilayer streak. The results indicate that LPS insertion causes net lipid flow from the broad bilayer region to the streak area. The differential increase in area is explained by the instability of planar bilayer streaks that originate from the large energetic contribution of line tension arising along the bilayer edge.