ArticlePloS one2014
Poly(ethylene glycol)-cholesterol inhibits L-type Ca2+ channel currents and augments voltage-dependent inactivation in A7r5 cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- The Slo1 Y450F Substitution Modifies Basal Function and Cholesterol Response of Middle Cerebral Artery Smooth Muscle BK Channels in a Sexually Dimorphic Manner.International journal of molecular sciences · 2025Article
- Glucose-6-phosphate dehydrogenase increases CaAmerican journal of physiology. Heart and circulatory physiology · 2020Article
- Dehydroepiandrosterone inhibits IAmerican journal of physiology. Heart and circulatory physiology · 2018Article
- Rotenone-stimulated superoxide release from mitochondrial complex I acutely augments L-type Ca2+ current in A7r5 aortic smooth muscle cells.American journal of physiology. Heart and circulatory physiology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
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 ICa,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.
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Registered trials
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