scholarly journals Diffusion in phospholipid bilayer membranes: dual-leaflet dynamics and the roles of tracer–leaflet and inter-leaflet coupling

Author(s):  
Reghan J. Hill ◽  
Chih-Ying Wang

A variety of observations—sometimes controversial—have been made in recent decades when attempting to elucidate the roles of interfacial slip on tracer diffusion in phospholipid membranes. Evans–Sackmann theory (1988) has furnished membrane viscosities and lubrication-film thicknesses for supported membranes from experimentally measured lateral diffusion coefficients. Similar to the Saffman and Delbrück model, which is the well-known counterpart for freely supported membranes, the bilayer is modelled as a single two-dimensional fluid. However, the Evans–Sackman model cannot interpret the mobilities of monotopic tracers, such as individual lipids or rigidly bound lipid assemblies; neither does it account for tracer–leaflet and inter-leaflet slip. To address these limitations, we solve the model of Wang and Hill, in which two leaflets of a bilayer membrane, a circular tracer and supports are coupled by interfacial friction, using phenomenological friction/slip coefficients. This furnishes an exact solution that can be readily adopted to interpret the mobilities of a variety of mosaic elements—including lipids, integral monotopic and polytopic proteins, and lipid rafts—in supported bilayer membranes.

2013 ◽  
Vol 723 ◽  
pp. 352-373 ◽  
Author(s):  
Chih-Ying Wang ◽  
Reghan J. Hill

AbstractWe model a cylindrical inclusion (lipid or membrane protein) translating with velocity$U$in a thin planar membrane (phospholipid bilayer) that is supported above and below by Brinkman media (hydrogels). The total force$F$, membrane velocity, and solvent velocity are calculated as functions of three independent dimensionless parameters:$\Lambda = \eta a/ ({\eta }_{m} h)$,${\ell }_{1} / a$and${\ell }_{2} / a$. Here,$\eta $and${\eta }_{m} $are the solvent and membrane shear viscosities,$a$is the particle radius,$h$is the membrane thickness, and${ \ell }_{1}^{2} $and${ \ell }_{2}^{2} $are the upper and lower hydrogel permeabilities. As expected, the dimensionless mobility$4\mathrm{\pi} \eta aU/ F= 4\mathrm{\pi} \eta aD/ ({k}_{B} T)$(proportional to the self-diffusion coefficient,$D$) decreases with decreasing gel permeabilities (increasing gel concentrations), furnishing a quantitative interpretation of how porous, gel-like supports hinder membrane dynamics. The model also provides a means of inferring hydrogel permeability and, perhaps, surface morphology from tracer diffusion measurements.


1986 ◽  
Vol 49 (4) ◽  
pp. 849-856 ◽  
Author(s):  
B. Goins ◽  
M. Masserini ◽  
B.G. Barisas ◽  
E. Freire

1987 ◽  
Vol 65 (2) ◽  
pp. 238-244 ◽  
Author(s):  
N. O. Petersen ◽  
R. Gratton ◽  
E. M. Pisters

The fluorescence characteristics of the polyene antibiotic Nystatin have been studied by measurements of quantum yields, lifetimes, and anisotropies in a model bilayer membrane. These measurements have been performed as a function of temperature and fluorophore-to-phospholipid molar ratio. Comparisons with data available for the parinaric acids demonstrate that the photophysics of the two polyene chromophores is similar. The quantum yield decreases at increasing Nystatin densities while the lifetimes are constant. These observations combined with quantitative comparisons with calculations of the density dependence of dynamic quenching in two-dimensional systems show that Nystatin fluorescence is quenched in bilayer membranes by a static process. This is likely due to the formation of complexes within the bilayer. The quenching is equally efficient in both the gel and liquid crystalline phases of the bilayer which suggests that the formation of the complexes occurs at all temperatures. At high Nystatin densities, there is also a quenching of the polarization, but the mechanism whereby this occurs is not clear. The limiting anisotropy at low concentrations is between 0.33 and 0.35 at all temperatures, suggesting that the Nystatin monomer is highly restricted in its reorientational motion in both gel and liquid crystalline phases.


1980 ◽  
Vol 75 (3) ◽  
pp. 241-250 ◽  
Author(s):  
J Zimmerberg ◽  
F S Cohen ◽  
A Finkelstein

Multilamellar phospholipid vesicles are introduced into the cis compartment on one side of a planar phospholipid bilayer membrane. The vesicles contain a water-soluble fluorescent dye trapped in the aqueous phases between the lamellae. If a vesicle containing n lamellae fuses with a planar membrane, an n-1 lamellar vesicle should be discharged into the opposite trans compartment, where it would appear as a discernible fluorescent particle. Thus, fusion events can be assayed by counting the number of fluorescent particles appearing in the trans compartment. In the absence of divalent cation, fusion does not occur, even after vesicles have been in the cis compartment for 40 min. When CaCl2 is introduced into the cis compartment to a concentration of greater than or equal to 20 mM, fusion occurs within the next 20 min; it generally ceases thereafter because of vesicle aggregation in the cis compartment. With approximately 3 x 10(8) vesicles/cm3 in the cis compartment, about 25-50 fusion events occur following CaCl2 addition. The discharge of vesicular contents across the planar membrane is the most convincing evidence of vesicle-membrane fusion and serves as a model for that ubiquitous biological phenomenon--exocytosis.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Koshi Nishida ◽  
Toshifumi Tojo ◽  
Takeshi Kondo ◽  
Makoto Yuasa

AbstractPorphyrin derivatives accumulate selectively in cancer cells and are can be used as carriers of drugs. Until now, the substituents that bind to porphyrins (mainly at the meso-position) have been actively investigated, but the effect of the functional porphyrin positions (β-, meso-position) on tumor accumulation has not been investigated. Therefore, we investigated the correlation between the functional position of substituents and the accumulation of porphyrins in cancer cells using cancer cells. We found that the meso-derivative showed higher accumulation in cancer cells than the β-derivative, and porphyrins with less bulky substituent actively accumulate in cancer cells. When evaluating the intracellular distribution of porphyrin, we found that porphyrin was internalized by endocytosis and direct membrane permeation. As factors involved in these two permeation mechanisms, we evaluated the affinity between porphyrin-protein (endocytosis) and the permeability to the phospholipid bilayer membrane (direct membrane permeation). We found that the binding position of porphyrin affects the factors involved in the transmembrane permeation mechanisms and impacts the accumulation in cancer cells.


2000 ◽  
Vol 12 (1) ◽  
pp. 13-22
Author(s):  
Stephen L. De Wall ◽  
Eric S. Meadows ◽  
Clare L. Murray ◽  
Hossein Shabany ◽  
George W. Gokel

1980 ◽  
Vol 75 (3) ◽  
pp. 251-270 ◽  
Author(s):  
F S Cohen ◽  
J Zimmerberg ◽  
A Finkelstein

Fusion of multilamellar phospholipid vesicles with planar phospholipid bilayer membranes was monitored by the rate of appearance in the planar membrane of an intrinsic membrane protein present in the vesicle membranes. An essential requirement for fusion is an osmotic gradient across the planar membrane, with the cis side (the side containing the vesicles) hyperosmotic to the opposite (trans) side; for substantial fusion rates, divalent cation must also be present on the cis side. Thus, the low fusion rates obtained with 100 mM excess glucose in the cis compartment are enhanced orders of magnitude by the addition of 5-10 mM CaCl2 to the cis compartment. Conversely, the rapid fusion rates induced by 40 mM CaCl2 in the cis compartment are completely suppressed when the osmotic gradient (created by the 40 mM CaCl2) is abolished by addition of an equivalent amount of either CaCl2, NaCl, urea, or glucose to the trans compartment. We propose that fusion occurs by the osmotic swelling of vesicles in contact with the planar membrane, with subsequent rupture of the vesicular and planar membranes in the region of contact. Divalent cations catalyze this process by increasing the frequency and duration of vesicle-planar membrane contact. We argue that essentially this same osmotic mechanism drives biological fusion processes, such as exocytosis. Our fusion procedure provides a general method for incorporating and reconstituting transport proteins into planar phospholipid bilayer membranes.


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