Human aortic endothelial cells studies with

Growing clinical data also points to the importance of IL-8 in atherogenesis. IL-8 has been found in atheromatous lesions from patients with atherosclerotic disease including carotid artery stenosis (103), CAD (118), abdominal aortic aneurysms (AAA) (103,104,114), and peripheral vascular disease (PVD) (104). Furthermore, studies using plaque explant samples have yielded more direct evidence for IL-8 involvement. Media from cultured AAA tissue induced IL-8-dependent human aortic endothelial cell (HAEC) chemotaxis (122). Homocysteine, implicated as a possible biomarker for CAD, is also capable of inducing IL-8 (123-125) by direct stimulation of endothelial cells (123,124) and monocytes (125). When patients with hyperhomocysteinemia were treated with low-dose folic acid, decreases in homocysteine levels correlated with decreases in IL-8 levels (126). Statins significantly decrease serum levels of IL-6, IL-8, and MCP-1, as well as expression of IL-6, IL-8, and MCP-1 mRNA by peripheral blood monocytes and HUVECs (127). Thus, IL-8 may be an underappreciated factor in the pathogenesis of atherosclerosis. 

Studies with Human Aortic Endothelial Cell (HAEC). 155... 

This chapter summarizes our recent studies on resveratrol, with regard to its effects on(l) oxidation of low-density lipoprotein (LDL), (2) cells effecting development of the AS, and (3) experiments using hypercholesterolemic rabbits. Furthermore, we report preliminary results of the effects of resveratrol in human aortic endothelial cells (HAEC). In these cells, RT-PCR analysis shows that resveratrol elicits an increase in p38 MAP kinase, concomitant with significant induction of heat shock protein 27 (Hsp27). We hypothesize that resveratrol may confer cardioprotection by functioning as a pleiotropic cellular effector. 

STUDIES WITH HUMAN AORTIC ENDOTHELIAL CELL (HAEC)... 

Garcia-Cardena reported in 1996 that the tyrosine phosphorylation of eNOS in bovine aortic endothelial cells (BAEC) resulted in a decrease in enzyme activity whilst immunoprecipitation of caveolin-1, the predominant isoform in endothelial cells, resulted in co-immunoprecipitation of tyrosine phosphorylated eNOS [17]. Michel et al. (1997) further reported that eNOS, also in BAEC, was co-immunoprecipitaed by caveolin-1 antibodies whilst in rat myocytes eNOS was associated with caveolin-3, the cardiac muscle specific type, confirming that eNOS interaction with caveolin is not tissue specific [18]. Immunofluoresence studies in our group have shown that eNOS associates with caveolin-1 in human umbilical vein endothelial cells (HUVEC), and this interaction is abolished by bradykinin (Wyatt, Pedley Mann, 2001 unpublished data) (Figure 3). 

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