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- W3173380211 abstract "Previous studies support a role for caveolin-1 (cav-1) dysfunction in membrane depolarization-induced Ca2+ sensitization in pulmonary vascular smooth muscle (VSM) from rats exposed to chronic hypoxia (CH). Because caveolar cholesterol content is important in regulation of cav-1-protein interactions, we hypothesized that reduced membrane cholesterol contributes to enhanced Ca2+ sensitivity following CH. We therefore examined vasoconstrictor responses to depolarizing concentrations of KCl (30–120 mM) under VSM Ca2+-clamp conditions following administration of supplemental cholesterol [500 μM - 5 mM methyl-β-cyclodextrin (MβCD)], or cholesterol depletion (MβCD, 10 mM) in pressurized endothelium-disrupted pulmonary arteries (~150 μm diameter) from control and CH (4 wk at 0.5 atm) rats. Consistent with our hypothesis, cholesterol repletion decreased KCl-dependent constriction in CH arteries and normalized reactivity between groups, while MβCD had no effect in either group. Additionally, CH reduced membrane cholesterol content as determined by filipin fluorescence. However, CH did not affect either arterial cav-1 levels or caveolar density assessed by western blot and electron microscopy, respectively. We conclude that decreased membrane cholesterol is necessary but not sufficient for enhanced depolarization-induced pulmonary VSM Ca2+- sensitization following CH." @default.
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- W3173380211 date "2012-04-01" @default.
- W3173380211 modified "2023-10-16" @default.
- W3173380211 title "Decreased membrane cholesterol facilitates depolarizationinduced Ca 2+ ‐sensitization in pulmonary vascular smooth muscle following chronic hypoxia" @default.
- W3173380211 doi "https://doi.org/10.1096/fasebj.26.1_supplement.873.14" @default.
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