Membrane cholesterol modulates dihydropyridine receptor function in mice fetal skeletal muscle cells

Pouvreau, Stéphane; Berthier, Christine; Blaineau, S.; Amsellem, Jacqueline; Coronado, Roberto; Strube, Caroline

doi:10.1113/jphysiol.2003.055285

Cited by 48 publications

(58 citation statements)

References 82 publications

(102 reference statements)

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“…We studied the effect of MbCD, which has been widely used as a membrane cholesterol depleting agent, 14,[20][21][22][23][24]28,29 on the localization of WT-Kv11.1 protein in the different sucrose gradient membrane fractions. HEK293 cells over-expressing WT-Kv11.1 channels were treated with and without 10 mM MbCD for 15 min and sucrose gradient membrane fractions were isolated, and we measured the cholesterol and protein concentrations in each sucrose gradient fraction.…”

Section: Resultsmentioning

confidence: 99%

“…Cyclodextrins are cyclic oligomers of glucose that sequester lipophiles in their hydrophobic core, thereby enhancing cholesterol solubility in aqueous solution. [25][26][27] In cell culture systems MbCD has been shown to remove cholesterol from cell membranes, 14,20,21,27 whereas cholesterol + MbCD loads cell membranes, 20,23,24,28,29 thus cyclodextrins can function as efficient acceptors and donors of cholesterol. For cholesterol depletion a final concentration of 10 mM MbCD was used, and for the cholesterol loading of cells, cholesterol + MbCD with a molar ratio of cholesterol/MbCD of 1/5 at a final concentration of 10 mM MbCD was used.…”

Section: Methodsmentioning

confidence: 99%

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Kv11.1 (ERG1) K⁺Channels Localize in Cholesterol and Sphingolipid Enriched Membranes and Are Modulated by Membrane Cholesterol

Balijepalli

Delisle²,

Balijepalli³

et al. 2007

Channels

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Kv11.1 (ERG1) K⁺Channels Localize in Cholesterol and Sphingolipid Enriched Membranes and Are Modulated by Membrane Cholesterol

Balijepalli

Delisle²,

Balijepalli³

et al. 2007

Channels

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“…Interestingly a recent study using the cholesterol-depleting agent methyl-β-cyclodextrin showed no change in membrane capacitance or t-tubule structure in rat ventricular myocytes (Calaghan & White, 2006), although previous work has shown that methyl-β-cyclodextrin disrupts the t-tubules in myotubes (Pouvreau et al, 2004), so that the structure of skeletal and cardiac t-tubules may rely to different extents on cholesterol. It might be expected, however, that insertion of cholesterol in the membrane would increase membrane thickness, and thus decrease capacitance.…”

Section: Effect Of Cholesterol On Membrane Capacitancementioning

confidence: 94%

Quantification of t-tubule area and protein distribution in rat cardiac ventricular myocytes

Pásek

Brette

Nelson

et al. 2008

Progress in Biophysics and Molecular Biology

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The transverse (t-) tubules of cardiac ventricular myocytes are invaginations of the surface membrane that form a complex network within the cell. Many of the key proteins involved in excitation-contraction coupling appear to be located predominantly at the t-tubule membrane.Despite their importance, the fraction of cell membrane within the t-tubules remains unclear: measurement of cell capacitance following detubulation suggests ~32%, whereas optical measurements suggest up to ~65%. We have therefore investigated the factors that may account for this discrepancy. Calculation of the combinations of t-tubule radius, length and density that produce t-tubular membrane fractions of 32% or 56% suggest that the true fraction is at the upper end of this range. Assessment of detubulation using confocal and electron microscopy suggests that incomplete detubulation can account for some, but not all of the difference. High cholesterol, and a consequent decrease in specific capacitance, in the t-tubule membrane, may also cause the ttubule fraction calculated from the loss of capacitance following detubulation to be underestimated. Correcting for both of these factors results in an estimate that is still lower than that obtained from optical measurements suggesting either that optical methods overestimate the fraction of membrane in the t-tubules, or that other, unknown, factors, reduce the apparent fraction obtained by detubulation. A biophysically realistic computer model of a rat ventricular myocyte, incorporating a t-tubule network, is used to assess the effect of the altered estimates of t-tubular membrane fraction on the calculated distribution of ion flux pathways.

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“…High cholesterol and sphingolipid concentrations in the plasma membrane are associated with discrete membrane domains [29] that are enriched with caveolins. The extraction of cholesterol from skeletal muscle fibre diminishes the interaction of caveolin-3 with dystrophin [30] and affects the contraction force of the muscle [31]. Because TT-membranes are enriched in cholesterol, cholesterol depletion may alter muscle mechanical activity by affecting the activity of the dihydropyridine receptor [31].…”

Section: Introductionmentioning

confidence: 99%

Cholesterol Depletion Uncouples �-dystroglycans from Discrete Sarcolemmal Domains, Reducing the Mechanical Activity of Skeletal Muscle

Vega-Moreno

Tirado-Cortés²,

Álvarez³

et al. 2012

Cell Physiol Biochem

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Background/Aims: β-Dystroglycan (β-DG) is a transmembrane glycoprotein that links the intracellular cytoskeleton to the extracellular matrix and is crucial for the molecular pathway of lateral force transmission in muscle. We aimed to investigate the effect of decreasing sarcolemmal cholesterol on the distribution of β-DG, its interaction with dystrophin and the impact on the contraction efficiency of muscle. Methods: Isolated rat extensor digitorum longus muscles were incubated with methyl β-cyclodextrin (MβCD) to deplete cholesterol and with MβCD-cholesterol to restore cholesterol. Electric stimulation protocols were used to determine muscle force and fatigue. Detergent-resistant membranes (lipid rafts) were separated from isolated skeletal muscle sarcolemma. The distribution and interactions of β-DG, caveolin-3 and dystrophin were determined by an immunoreactivity analysis. Results: Cholesterol depletion in muscle results in a weakened force of contraction, which recovers after cholesterol restoration. The rate of fatigue is unaffected, but fatigue recovery is dependent upon cholesterol restoration. MβCD modifies the structures of lipid rafts obtained from MβCD-treated muscles by, displacing the membrane proteins β-DG and caveolin-3 f from the lipid raft, thus reducing the interaction of β-DG with dystrophin. Conclusion: Cholesterol depletion weakens the muscle contractile force by disturbing the sarcolemmal distribution of β-dystroglycan and its interaction with dystrophin, two key proteins in the alignment of lateral force transmission pathway.

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Membrane cholesterol modulates dihydropyridine receptor function in mice fetal skeletal muscle cells

Cited by 48 publications

References 82 publications

Kv11.1 (ERG1) K⁺Channels Localize in Cholesterol and Sphingolipid Enriched Membranes and Are Modulated by Membrane Cholesterol

Kv11.1 (ERG1) K⁺Channels Localize in Cholesterol and Sphingolipid Enriched Membranes and Are Modulated by Membrane Cholesterol

Quantification of t-tubule area and protein distribution in rat cardiac ventricular myocytes

Cholesterol Depletion Uncouples �-dystroglycans from Discrete Sarcolemmal Domains, Reducing the Mechanical Activity of Skeletal Muscle

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Membrane cholesterol modulates dihydropyridine receptor function in mice fetal skeletal muscle cells

Cited by 48 publications

References 82 publications

Kv11.1 (ERG1) K+Channels Localize in Cholesterol and Sphingolipid Enriched Membranes and Are Modulated by Membrane Cholesterol

Kv11.1 (ERG1) K+Channels Localize in Cholesterol and Sphingolipid Enriched Membranes and Are Modulated by Membrane Cholesterol

Quantification of t-tubule area and protein distribution in rat cardiac ventricular myocytes

Cholesterol Depletion Uncouples �-dystroglycans from Discrete Sarcolemmal Domains, Reducing the Mechanical Activity of Skeletal Muscle

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Kv11.1 (ERG1) K⁺Channels Localize in Cholesterol and Sphingolipid Enriched Membranes and Are Modulated by Membrane Cholesterol

Kv11.1 (ERG1) K⁺Channels Localize in Cholesterol and Sphingolipid Enriched Membranes and Are Modulated by Membrane Cholesterol