Key result
Lipid raft disruption with methyl-β-cyclodextrin shifted the midpoint of activation of HCN4 current in HEK cells and If in SAN cells to the positive direction by 11.9 and 10.4 mV, respectively.
Why the study?
Does lipid raft disruption by MβCD alter the localization and kinetics of HCN4 pacemaker channels in HEK and rabbit SAN cells?
Population
HEK cells expressing HCN4 channels and rabbit sinoatrial (SAN) cells
Comparison
Lipid raft disruption by cell incubation with… vs Untreated cells
Design
Preclinical
Authors
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Lipid raft integrity modulates HCN4 gating in vitro; leaves open whether raft-targeted interventions could alter sinus node function in vivo.
Does lipid raft disruption by MβCD alter the localization and kinetics of HCN4 pacemaker channels in HEK and rabbit SAN cells?
Effect estimate: shifted to the positive direction by 11.9 and 10.4 mV, respectively
Pacemaker channels localize to lipid rafts, and disruption of these rafts alters channel distribution and modifies their kinetic properties, increasing pacemaker activity.
Barbuti et al. (2004) studied this question. Methyl-β-cyclodextrin (MβCD) was evaluated on Midpoint of activation of the HCN4 current in HEK cells and of If in SAN cells (shifted to the positive direction by 11.9 and 10.4 mV, respectively). Lipid raft disruption with methyl-β-cyclodextrin shifted the midpoint of activation of HCN4 current in HEK cells and If in SAN cells to the positive direction by 11.9 and 10.4 mV, respectively.
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