sn-Glycero-3-phosphocholine

Polarized attenuated total reflection (ATR-IR) spectroscopy and fluorescence microscopy techniques were used to characterize a 1,2-diphytanoyl-sn-glycero-3-phosphocholine (DPhPC) membrane supported on porous, cationic hydrogel beads. Fluorescence microscopy images showed that the DPhPC coated the external surface of the hydrogel scaffold. In addition, a fluorescence assay of the emission intensity of the Tb3+/dipicolinic acid complex demonstrated that the DPhPC coating acted as a barrier to Tb3+ efflux from the scaffolded vesicle and successfully sealed the porous hydrogel bead. Fluorescence quenching and ATR-IR spectroscopic measurements revealed that the lipid coating has a bilayer structure. The phytanoyl chains were found to exhibit significant trans-gauche isomerization, characteristic of the fluid liquid phase. However, no lipid lateral mobility was observed by fluorescence recovery after photobleaching (FRAP) measurements. The phosphocholine headgroup was found to be well hydrated and oriented such that the cationic choline group tucked in behind the anionic phosphate group, consistent with an electrostatic attraction between the cationic scaffold and zwitterionic lipid.

We investigate the phase transition stages for detergent-mediated liposome solubilization of bio-mimetic membranes with the motivation of integrating membrane-bound Photosystem I into bio-hybrid opto-electronic devices. To this end, the interaction of two non-ionic detergents n-dodecyl-β-D-maltoside (DDM) and Triton X-100 (TX-100) with two types of phospholipids, namely DPhPC (1,2-diphytanoyl-sn-glycero-3-phosphocholine) and DPPG (1,2-dipalmitoyl-sn-glycero-3-phospho-(1'-rac-glycerol)), are examined. Specifically, solubilization processes for large unilamellar liposomes are studied with the aid of turbidity measurements, dynamic light scattering, and cryo-transmission electron microscopy imaging. Our results indicate that the solubilization process is well depicted by a three-stage model, wherein the lamellar-to-micellar transitions for DPhPC liposomes are dictated by the critical detergent/phospholipid ratios. The solubilization of DPhPC by DDM is devoid of formation of a "gel-like" phase.

We investigate a temperature-driven recursive division of binary giant unilamellar vesicles (GUVs). During the heating step of the heating-cooling cycle, the spherical mother vesicle deforms to a budded limiting shape using up the excess area produced by the chain melting of the lipids and then splits off into two daughter vesicles. Upon cooling, the daughter vesicle opens a pore and recovers the spherical shape of the mother vesicle. Our GUVs are composed of DLPE (1,2-dilauroyl-sn-glycero-3-phosphoethanolamine) and DPPC (1,2-dipalmitoyl-sn-glycero-3-phosphocholine). During each cycle, vesicle deformation is monitored by a fast confocal microscope and the images are analyzed to obtain the time evolution of reduced volume and reduced monolayer area difference as the key geometric parameters that quantify vesicle shape. By interpreting the deformation pathway using the area-difference elasticity theory, we conclude that vesicle division relies on (1) a tiny asymmetric distribution of DLPE within the bilayer, which controls the observed deformation from the sphere to the budded shape; and (2) redistribution of DLPE during the deformation-division stage, which ensures that the process is recursive.

Lipid mediators of inflammation play important roles in several diseases including skin cancer, the most prevalent type of cancer found in the industrialized world. Ultraviolet (UV) radiation is a complete carcinogen and is the primary cause of skin cancer. UV radiation is also a potent immunosuppressive agent, and UV-induced immunosuppression is a well-known risk factor for skin cancer induction. An essential mediator in this process is the glyercophosphocholine 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine commonly referred to as platelet-activating factor (PAF). PAF is produced by keratinocytes in response to diverse stimuli and exerts its biological effects by binding to a single specific G-protein-coupled receptor (PAF-R) expressed on a variety of cells. This review will attempt to describe how this lipid mediator is involved in transmitting the immunosuppressive signal from the skin to the immune system, starting from its production by keratinocytes, to its role in activating mast cell migration in vivo, and to the mechanisms involved that ultimately lead to immune suppression.