PMID: 9554975May 23, 1998Paper

Elevation of cyclic AMP by iloprost and prostaglandin E1 increases cholesterol efflux and the binding capacity for high-density lipoproteins in human fibroblasts

Biochimica Et Biophysica Acta
A Middleton, B Middleton

Abstract

Elevation of cAMP concurrently enhances cholesterol efflux and binding of HDL3 in human skin fibroblasts. These effects were observed regardless of the route by which cAMP levels were increased. Cholesterol efflux and HDL3 binding were stimulated by the cAMP analogue CPT-cAMP, the adenylate cyclase activator forskolin, and by iloprost and prostaglandin E1 (PGE1) (which elevate cAMP via receptor-mediated processes). Dideoxyforskolin and PGF2alpha, which do not elevate cAMP, altered neither cholesterol efflux nor binding of HDL3. Inhibition of protein kinase A with H89 abolished the stimulatory effects of CPT-cAMP and iloprost, suggesting protein kinase A involvement in enhancing cholesterol efflux and HDL3 binding. Enhancement of HDL3 binding by iloprost was due to increased maximal capacity of the cells to bind HDL3, i.e., a greater number of HDL3 binding sites. A positive correlation was demonstrated between changes in HDL3 binding and changes in [3H]cholesterol efflux. The data are compatible with a model in which cholesterol efflux is partially dependent upon HDL binding to the cells. A short exposure to iloprost was sufficient to stimulate cAMP synthesis, triggering a chain of events leading to increased HDL3 binding and [3...Continue Reading

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Citations

Jul 17, 1999·Atherosclerosis·O Stein, Y Stein
Sep 29, 1999·Proceedings of the National Academy of Sciences of the United States of America·Y Takahashi, J D Smith
Sep 22, 2007·Advanced Drug Delivery Reviews·Dehai LiangBenjamin Chu
Oct 26, 2010·Journal of Biomaterials Applications·Chennakkattu Krishna Sadasivan Pillai, Chandra P Sharma
Feb 24, 2001·Bioscience, Biotechnology, and Biochemistry·K KobaY S Huang

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