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Cholesterol distributes at a high density in the membrane lipid raft and modulates ion channel currents. Poly(ethylene glycol) cholesteryl ether (PEG-cholesterol) is a nonionic amphipathic lipid consisting of lipophilic cholesterol and covalently bound hydrophilic PEG. PEG-cholesterol is used to formulate lipoplexes to transfect cultured cells, and liposomes for encapsulated drug delivery. PEG-cholesterol is dissolved in the external leaflet of the lipid bilayer, and expands it to flatten the caveolae and widen the gap between the two leaflets. We studied the effect of PEG-cholesterol on whole cell L-type Ca 2+  channel currents ( I   Ca,L ) recorded from cultured A7r5 arterial smooth muscle cells. The pretreatment of cells with PEG-cholesterol decreased the density of  I   Ca,L  and augmented the voltage-dependent inactivation with acceleration of time course of inactivation and negative shift of steady-state inactivation curve. Methyl-β-cyclodextrin (MβCD) is a cholesterol-binding oligosaccharide. The enrichment of cholesterol by the MβCD:cholesterol complex (cholesterol (MβCD)) caused inhibition of  I   Ca,L  but did not augment voltage-dependent inactivation. Incubation with MβCD increased  I   Ca,L , slowed the time course of inactivation and shifted the inactivation curve to a positive direction. Additional pretreatment by a high concentration of MβCD of the cells initially pretreated with PEG-cholesterol, increased  I   Ca,L  to a greater level than the control, and removed the augmented voltage-dependent inactivation. Due to the enhancement of the voltage-dependent inactivation, PEG-cholesterol inhibited window  I   Ca,L  more strongly as compared with cholesterol (MβCD). Poly(ethylene glycol) conferred to cholesterol the efficacy to induce sustained augmentation of voltage-dependent inactivation of  I   Ca,L .

Poly(Ethylene Glycol)-Cholesterol Inhibits L-Type Ca2+ Channel Currents and Augments Voltage-Dependent Inactivation in A7r5 Cells