Interrogating the role of liposome size in mediating the dynamics of a chromophore in the acyl chain region of a phospholipid bilayer

Lapinski, Monique M.; Blanchard, G. J.

doi:10.1016/j.chemphyslip.2008.03.005

Cited by 14 publications

(29 citation statements)

References 50 publications

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“…For systems characterized by significant curvature, it is reasonable to expect morphology that is similar to that seen for a planar bilayer, but characterized by more facile exchange dynamics because of the structural freedom available to constituents of the bilayer leaflets. 32 This expectation is realized for the system examined here. For the planar bilayer structure we are able to resolve discrete populations of chromophore that do not exchange on the timescale of the chromophore motion, while for vesicles we observe a single exponential decay time constant that is the weighted average of the two time constants seen for the planar bilayer.…”

Section: Resultsmentioning

confidence: 52%

Interface-mediation of lipid bilayer organization and dynamics

Mize

Blanchard

2016

Phys. Chem. Chem. Phys.

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We report on the morphology and dynamics of planar supported lipid bilayer structures as a function of pH and ionic strength of the aqueous overlayer. Supported lipid bilayers composed of three components (phosphocholine, sphingomyelin and cholesterol) are known to exhibit phase segregation, with the characteristic domain sizes dependent on the amount and identity of each constituent, and the composition of the aqueous overlayer in contact with the bilayer. We report on fluorescence anisotropy decay imaging measurements of a rhodamine chromophore tethered to the headgroup of a phosphoethanolamine, where anisotropy decay images were acquired as a function of solution overlayer pH and ionic strength. The data reveal a two-component anisotropy decay under all conditions, with the faster time constant being largely independent of pH and ionic strength and the slower component depending on pH and ionic strength in different manners. For liposomes of the same composition, a single exponential anisotropy decay was seen. We interpret this difference in terms of bilayer curvature and support surface-bilayer interactions, and the pH and ionic strength dependencies in terms of ionic screening and protonation in the bilayer headgroup region.

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Section: Resultsmentioning

confidence: 52%

Interface-mediation of lipid bilayer organization and dynamics

Mize

Blanchard

2016

Phys. Chem. Chem. Phys.

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“…To measure membrane viscosity, we labeled synthetic vesicles with a fluorescent probe, perylene (Fig. A)—nonpolar polycyclic aromatic hydrocarbon that incorporates selectively into bilayer nonpolar region with well‐characterized rotational diffusion behavior . Viscosity of extruded synthetic vesicles was quantitated by rotational diffusion of perylene.…”

Section: Resultsmentioning

confidence: 99%

“…Constituents were present in chloroform or ethanol (perylene), aliquots were evaporated to dryness and taken up in 2.86 mL milli‐Q water. The mixture was put through five freeze‐thaw‐vortex cycles and extruded 11 times through a polycarbonate filter . The extruded vesicles were measured by DLS and were approximately 200 nm in diameter.…”

Section: Methodsmentioning

confidence: 99%

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Role of Acid Sphingomyelinase in Shifting the Balance Between Proinflammatory and Reparative Bone Marrow Cells in Diabetic Retinopathy

et al. 2016

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The metabolic insults associated with diabetes lead to low-grade chronic inflammation, retinal endothelial cell damage, and inadequate vascular repair. This is partly due to the increased activation of bone marrow (BM)-derived proinflammatory monocytes infiltrating the retina, and the compromised function of BM-derived reparative circulating angiogenic cells (CACs), which home to sites of endothelial injury and foster vascular repair. We now propose that a metabolic link leading to activated monocytes and dysfunctional CACs in diabetes involves upregulation of a central enzyme of sphingolipid signaling, acid sphingomyelinase (ASM). Selective inhibition of ASM in the BM prevented diabetes-induced activation of BM-derived microglia-like cells and normalized proinflammatory cytokine levels in the retina. ASM upregulation in diabetic CACs caused accumulation of ceramide on their cell membrane, thereby reducing membrane fluidity and impairing CAC migration. Replacing sphingomyelin with ceramide in synthetic membrane vesicles caused a similar decrease in membrane fluidity. Inhibition of ASM in diabetic CACs improved membrane fluidity and homing of these cells to damaged retinal vessels. Collectively, these findings indicate that selective modulation of sphingolipid metabolism in BM-derived cell populations in diabetes normalizes the reparative/proinflammatory cell balance and can be explored as a novel therapeutic strategy for treating diabetic retinopathy.

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“…In this study, the traditional Chinese herb, magnolol, was modified by different acyl chain lengths liposome. Liposomes are selfassembled and colloidal vesicles which commonly consist of phospholipids bilayers enclosing an aqueous solution, so that liposomes can carry both hydrophobic and hydrophilic molecules (Drummond et al, 2008;Lapinski and Blanchard, 2008;Sholto and Ehrenberg, 2008;Suwalsky et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Magnolol encapsulated by different acyl chain length of liposomes on inhibiting proliferation of smooth muscle cells

Chen

2009

Journal of the Taiwan Institute of Chemical Engineers

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Interrogating the role of liposome size in mediating the dynamics of a chromophore in the acyl chain region of a phospholipid bilayer

Cited by 14 publications

References 50 publications

Interface-mediation of lipid bilayer organization and dynamics

Interface-mediation of lipid bilayer organization and dynamics

Role of Acid Sphingomyelinase in Shifting the Balance Between Proinflammatory and Reparative Bone Marrow Cells in Diabetic Retinopathy

Magnolol encapsulated by different acyl chain length of liposomes on inhibiting proliferation of smooth muscle cells

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