Chemokine expression atherosclerosis with

In an animal model of atherosclerosis E2 restores FasL expression, which is suppressed by atherogenic levels of serum cholesterol (328). High levels of Hey diminish with estrogen (reviewed in ref. 329). In HUVEC, E2 caused a decrease in expression of the NADPH oxidase subunit gp91phox, up-regulated eNOS expression, and inhibited the increase in adhesion molecule and chemokine expression in cells exposed to cyclic strain. Cyclic strain enhanced endothelial 02 formation, thereby offsetting the inhibitory effect of NO on the expression of these gene products (330). 

Fig. 5. Scavenger receptors (SRs). Structural features of scavenger receptors with proposed roles in atherosclerosis. The plasma membrane or the endosomal membrane (for CD68, which is mainly found in the endosomal compartment) is indicated by the vertical line, with the cytoplasmic domains to the left. The individual structural domains are described in the box. SRCL, SR with C-type lectin MARCO, macrophage receptor with collagenous structure SREC, SR expressed by endothelial cells SR-PSOX/CXCL16, membrane-bound chemokine L16 other SRs are described in the text (Section 7). Not drawn to scale.

MCP-1 and chemokine receptor 2 (CCR2) play important roles in monocyte recruitment MCP-1 expression is increased in human atherosclerotic plaques, vascular endothelium, and VSMC exposed to minimally modified lipids. In Apo E deficient mice that lack CCR2, lesion formation was decreased with no effects on lipids (164) on the other hand, MCP-1 expression by leukocytes (macrophages) increases macrophage number and oxidized lipid accumulation and atherosclerosis progression in Apo E deficient MCP-1 transgenic mice, with no effects on plasma lipoprotein profile (165). However, local MCP-1 overexpression at the vessel is not sufficient in rabbits, and activation by other factors induced by hypercholesterolemia is required (166). 

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