Abstract
Acrucial event in atherosclerosis is the formation of foam cells. Vascular cell adhesion molecule-1 (VCAM-1), intercellular cell adhesion molecule-1 (ICAM-1), macrophage chemoattractant protein-1 (MCP-1), and macrophage colony stimulating factor (M-CSF) are important molecules that contribute to foam cell formation.1 Removal of excess free cholesterol from macrophages, neutralization of monocyte migration inhibitory factor (MIF), and reduction of proinflammatory cytokine concentrations are important goals for the prevention of foam cell formation and the development of atherosclerosis. 2,3 Increases in intracellular cAMP concentration inhibit the expression of ICAM-1 and VCAM-1, 4 decrease the production of MCP-1 5 and M-CSF, 6 increase the expression of antiinflammatory cytokines, and decrease the expression of MIF and proinflammatory interleukins. 7 In addition, cAMP analogs induce the ABCA1 secretory pathway, by which apolipoproteins (apoA-I) actively remove free cholesterol from cells; treatment of macrophages with cAMP analogs causes parallel increases in apo-I–mediated cholesterol efflux.8 On the basis of the role of cAMP in the expression of proatherogenic and antiatherogenic molecules, we postulated that the intracellular cAMP concentrations of peripheral monocytes may be low in patients with coronary artery
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