The cycle of cholesterol movement between cell-surface caveolae and intracellular pools rich in cholesterol contributes to caveolae cholesterol homeostasis. This cycle is controlled in a complex fashion that can involve scavenger receptors (SR-BI and CD-36), lipoproteins, and even sex hormones [11,14,65,77,78]. Many studies using methyl-beta-cyclodextrin have documented that cholesterol depletion and repletion cause major changes in the organization of caveolae, caveolin-1 localization to caveolae, or redistribution to intracellular sites, and resultant effects on numerous signaling proteins that are found in association with caveolae or bound to caveolae by caveolin-1. A recent report has shown that shear stress induction of eNOS activity is also susceptible to disruption of caveolae cholesterol, either by methylbeta cyclodextrin depletion, or by cyclosporine A inhibition of caveolin-1-cypA interaction . This indicates that disruption of this chaperone complex cycle contributes to the endothelial pathogenesis which leads to hypertension induced by cyclosporine.
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