Influence of brain gangliosides on the formation and properties of supported lipid bilayers

被引:13
|
作者
Jordan, Luke R. [1 ]
Blauch, Megan E. [1 ]
Baxter, Ashley M. [1 ]
Cawley, Jennie L. [1 ]
Wittenberg, Nathan J. [1 ]
机构
[1] Lehigh Univ, Dept Chem, 6 East Packer Ave, Bethlehem, PA 18015 USA
关键词
Ganglioside; Glycolipid; Supported lipid bilayer; Membrane; Quartz crystal microbalance; Fluorescence recovery after photobleaching; QUARTZ-CRYSTAL MICROBALANCE; CHOLERA-TOXIN BINDING; PHOSPHOLIPID-BILAYERS; VESICLE ADSORPTION; QCM-D; DIVALENT-CATIONS; GM1; SURFACE; ACID; GLYCOSPHINGOLIPIDS;
D O I
10.1016/j.colsurfb.2019.110442
中图分类号
Q6 [生物物理学];
学科分类号
071011 ;
摘要
Gangliosides are glycolipids that are enriched on the outer surface of cell membranes. Gangliosides are receptors for a number of signaling molecules and toxins, and therefore are often incorporated into biosensors. Many of these biosensors incorporate gangliosides into supported lipid bilayers which are formed by the spontaneous rupture of unilamellar vesicles on glass or SiO2 substrates. In this work, we used quartz crystal microbalance with dissipation monitoring (QCM-D) to investigate how the presence of the four major brain gangliosides (GM1, GD1a, GD1b, and GT1b) influences the process of supported lipid bilayer formation on SiO2 surfaces. We show that the rate of supported bilayer formation is dependent on both the charge and position of sialic acid moieties on ganglioside molecules. Additionally, Ca2+ can accelerate ganglioside-rich supported bilayer formation, but the degree of acceleration differs for vesicles containing different gangliosides. Fluorescence recovery after photobleaching measurements show that the presence of all gangliosides reduces lipid diffusion coefficients in a concentration-dependent manner, and that Ca2+ slows lipid diffusion in membranes with and without gangliosides. Finally, we use ganglioside-rich supported bilayers to measure binding constants for a GD1a-binding antibody that has similar properties to antibodies present in a variant of Guillain-Barre syndrome.
引用
收藏
页数:9
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