Human aortic endothelial cells

Navab, M., Imes, S.S., Hama, S.Y., Hough, G.P., Ross, L.A., Bork, R.W., Valente, A.J., Berliner, J.A., Drinkwater, D.C., Laks, H. and Fogelman, A.M. (1991). Monocyte transmigration induced by modification of low density lipoprotein in cocultures of human aortic endothelial cells is due to induction of monocyte chemotactic protein 1 synthesis and is abolished by high density lipoprotein. J. Clin. Invest. 88, 2039-2046. 

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. 

Szekanecz Z, Shah MR, Harlow LA, Pearce WH, Koch AE. Interleukin-8 and tumor necrosis factor-alpha are involved in human aortic endothelial cell migration. The possible role of these cytokines in human aortic aneurysmal blood vessel growth. Pathobiology 1994 62(3) 134-139. 

Poddar R, Sivasubramanian N, DiBello PM, Robinson K, Jacobsen DW. Homocysteine induces expression and secretion of monocyte chemoattractant protein-1 and interleukin-8 in human aortic endothelial cells implications for vascular disease. Circulation 2001 103(22) 2717-2723. 

Unlike Cu(II), free Mn(II) ions are not active in superoxide dismutation, but some Mn(II)-macrocycle complexes catalyze the dismutation of 02 and are biologically active (441). For example, complex 94 (SC-52608) inhibits neutrophil-mediated killing of human aortic endothelial cells in vitro, attenuates inflammation, protects against myo-... 

Koga, T. and Meydani, M., Effect of plasma metabolites of (+)-catechin and quercetin on monocyte adhesion to human aortic endothelial cells. Am. J. Clin. Nutr., 73, 941, 2001. 

Lotito SB, Frei B. 2006. Dietary flavonoids attenuate tumor necrosis factor -induced adhesion molecule expression in human aortic endothelial cells Structure-function relationships and activity after first pass metabolism. J Biol Chem 281 37102-37110. 

Schramm DD, Wang JF, Holt RR, Ensunsa JL, Gonsalves JL, Lazarus SA, Schmitz HH, German JB, Keen CL. 2001. Chocolate procyanidins decrease the leukotriene-prostacyclin ratio in humans and human aortic endothelial cells. Am J Clin Nutr 73 36-40. 

Zhang WJ, Frei B, Intracellular metal ion chelators inhibit TNFalpha-induced SP-I activation and adhesion molecule expression in human aortic endothelial cells, Free Radic Biol Med 2003 34(6) 674-682. 

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. 

In the first part of this paper we shall snmmarize onr previons studies of the effects of resveratrol on LDL oxidation, on cells participating in atherogenesis, and on aspects of hypercholesterolemia using rabbits as a model. In the second part, we shall report our preliminary studies of the effects of resveratrol on cultured human aortic endothelial cells (HAECs). The implications of onr findings will also be discussed briefly. 

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

Martin, A., Foxall, T., Blumberg, J. B., and Meydani, M. (1997) Vitamin E inhibits low-density lipoprotein-induced adhesion of monocytes to human aortic endothelial cells in vitro. Arterioscler Thromb Vase Biol 17,429-36. 

Wu, D., Koga, T., Martin, K. R., and Meydani, M. (1999) Effect of vitamin E on human aortic endothelial cell production of chemokines and adhesion to monocytes. Atherosclerosis 147,297-307. 

Devaraj S, Xu DY, et al. C-reactive protein increases plasminogen activator inhibitor-1 expression and activity in human aortic endothelial cells implications for the metabolic syndrome and atherothrom-bosis. Circulation 2003 107 398-404. 

Matsubara, M and Hasegawa, K, Benidipine, a dihydropyridine-calcium channel blocker, prevents lysophosphatidylcholine-induced injury and reactive oxygen species production in human aortic endothelial cells. Atherosclerosis 178 (2005) 57-66. 

By the same token, a flavonoid, 2-(3-amino-phenyl)-8-methoxy-chromene-4-one, markedly inhibited TNF-alpha induced vascular cell adhesion molecule-1 (VCAM-1) in a concentration-dependent fashion of human aortic endothelial cells, but had no effect on intercellular adhesion molecule-1 (ICAM-1) [192]. 

Morrow, V.A. FoufeUe, F. Connell, J.M. Petrie, J.R. Gould, G.W. Salt, I.P. Direct activation of AMP-activated protein kinase stimulates nitric-oxide synthesis in human aortic endothelial cells. J. Biol. Chem., 278, 31629-31639 (2003)... 

Inhibition of Neutrophil-Mediated Human Aortic Endothelial Cell Injury by Superoxide Dismutase Mimics... 

We have reported the observation that the Mn(ii)-based SOD mimics inhibit superoxide-mediated injury to human aortic endothelial cells. The amount of injury to human aortic endothelial cells was assessed by pre-labeling the cells with [ Crjchromate, which is released into the medium when the cells are injured. Superoxide was produced either by activated human neutrophils or by xanthine/xanthine oxidase. The amount of injury to cells was directly correlated to the amount of superoxide the cells were exposed to. 

Ziegelstein RC, Corda S, Pili R, Passaniti A, Lefer D, Zweier JL, Fraticelli A, Capogrossi MC Initial contact and subsequent adhesion of human neutrophils or monocytes to human aortic endothelial cells releases an endothelial intracellular calcium store. Circulation 1994 90 1899-1907. 

Kenny TP, Keen CL, Jones P, Kimg HJ, Schmitz HH, Gershwin ME (2004) Pentameric procyanidins isolated from Theobroma cacao seeds selectively downregulate ErbB2 in human aortic endothelial cells. Exp Biol Med (Maywood) 229 255-263... 

Markers of inflammation, especially CRP (measured with a highly sensitive technique, referred to as hs-CRP), have become the center of attention in recent years (22). This increased interest stems from several important observations made by Ridker and co-workers. Serum CRP has been shown to be an independent cardiovascular disease risk factor (23,24). High levels predict CAD death in healthy middle-aged men (25) and in patients with unstable CAD (26). In acute coronary syndromes, serum CRP concentrations correlate with the severity of endothelial dysfunction (27). In the CARE trial, subjects with elevated markers of inflammation (CRP and serum amyloid A > 90th percentile) were at high cardiovascular risk and responded best to pravastatin treatment in terms of cardiovascular risk reduction (28). The statin also reduced serum CRP concentrations (29). CRP co-incubated with LDL is readily taken up by macrophages, in contrast to native LDL, suggesting that CRP could promote foam cell formation (30). A link with endothelial dysfunction may be related to the fact that CRP decreases endothelial nitric oxide synthase (eNOS) expression and bioactivity in human aortic endothelial cells (31). 

Venugopal, S.K., Devaraj, S., Yuhanna, L, Shaul, P., and Jialal, I. (2002) Demonstration That C-Reactive Protein Decreases eNOS Expression and Bioactivity in Human Aortic Endothelial Cells, Circulation 106,1439-1441. 

Genove E, Shen C, Zhang S, Semino CE (2005) The effect of functionalized self-assembling peptide scaffolds on human aortic endothelial cell function. Biomaterials 26 3341-3351. doi 10.1016/j.biomaterials.2004.08.012... 

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