Monocyte adhesion

Monocyte adhesion - Oxydative burst in neutrophils f %°x tv <4L S> / % j - Diacylglycerol kinase - Protein phosphatase 2A (PP2A)... 

Schwartz D, Andalibi A, Chaverri-Almada L, et al. Role of the GRO family of chemokines in monocyte adhesion to MM-LDL-stimulated endothelium. J Clin Invest 1994 94(5) 1968-1973. 

Besides cholesterol efflux from arterial wall and its role in RCT, additional properties of HDL have been proposed for its protective anti-atherogenic activities. HDL protects vascular function by a number of potential alternative mechanisms, including inhibition of LDL oxidation [8,9], platelet aggregation and coagulation [10], and endothelial monocyte adhesion [11], as well as promotion of endothelial nitric oxide synthase (eNOS) [12], and prostacyclin synthesis [13-15]. The proposed alternate protective mechanisms for HDL are attractive but many of them lack validation under in vivo conditions. 

A more selective inhibition of NFkB can be achieved by transfecting cells with DNA coding for the natural inhibitor IkBo or a mutant IkB protein that lacks 36 N-terminal amino acids, and consequently becomes proteolysis resistant. In this way expression of adhesion molecules and monocyte adhesion and transmigration can be inhibited [87,88], The potentials and limitations of these latter types of therapy are however not fully understood as yet. Different transfection systems (adenoviral, retroviral, non-viral) are available for gene delivery purposes, all with their own potentials and restrictions. 

Red wine consumption in humans reduces TNF-a-induced adhesion of monocytes to endothelial cells ex vivo and is associated with the downregulation of monocyte adhesion molecules, in particular very late activation antigen-4 (VLA-4). Estruch et al. reported similar findings for VLA-4 and also showed that levels of MCP-1, VCAM-1, and ICAM-1 were decreased after red wine consumption. Interestingly, control studies with gin revealed no effect... 

Ludwig, A., Lorenz, M., Grimbo, N., Steinle, F., Meiners, S., Bartsch, C., Stangl, K., Baumann, G., and Stangl, V., The tea flavonoid epigallocatechin-3-gallate reduces cytokine-induced VCAM-1 expression and monocyte adhesion to endothelial cells, Biochem. Biophys. Res. Commun., 316, 659, 2004. 

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. 

Tsubosaka, Y., Murata, T., Yamada, K., Uemura, D., Hori, M., and Ozaki, H. (2010b). Halichlorine reduces monocyte adhesion to endothelium through the suppression of nuclear factor- activation. J. Pharmacol. Sci. 113,208-213. 

M. Shen, M. S. Wagner, D. G. Castner and T. A. Horbett, Multivariate surface analysis of plasma-deposited tetraglyme for reduction of protein adsorption and monocyte adhesion, Langmuir, 19(5), 2003, 1692-1699. 

Ferrero ME, Bertelli AE, Fulgenzi A, Pellegatta F, Corsi MM, Bonfrate M, Ferrara F, De Caterina R, Giovannini L, Bertelli A. 1998. Activity in vitro of resveratrol on granulocyte and monocyte adhesion to endothelium. Am J Clin Nutr 68 1208-1214. 

Shen M, Pan YV, Wagner MS, Hauch KD, Castner DG, Ratner BD, Horbett TA. Inhibition of monocyte adhesion and fibrinogen adsorption on glow discharge plasma deposited tetraethylene glycol dimethyl ether. Journal of Biomaterials Science, Polymer Edition 2001, 12, 961-978. 

Because the endothelium has important inhibitory effects on platelet aggregation, monocyte adhesion, and smooth muscle cell (SMC) proliferation, strategies to improve vascular healing after spontaneous or induced injury may improve clinical outcomes in the long-term (Fig. I). 

Ernsting, M.J., Labow, R.S., and Santerre, J.P. "Human monocyte adhesion onto RGD and PHSRN peptides delivered to the surface of a polycarbonate polyurethane using bioactive fluorinated surface modifiers". ] Biomed. Mater. Res. A 83A(3), 759-769 (2007). Ewbank, P.C., Nuding, G., Suenaga, H., McCullough, R.D., and Shinkai, S. "Amine functionalized polythiophenes Synthesis and formation of chiral, ordered structures on DNA substrates". Tetrahedron Lett 42(2), 155-157 (2001). 

Devaraj, S., Li, D., and Jialal, I. (1996) The effects of alpha tocopherol supplementation on monocyte function. Decreased lipid oxidation, interleukin 1 beta secretion, and monocyte adhesion to endothelium. J Clin Invest 98, 756-63. 

Williams, J. C., Forster, L. A., Tull, S. P., Wong, M., Bevan, R. J., and Ferns, G. A. (1997) Dietary vitamin E supplementation inhibits thrombin-induced platelet aggregation, but not monocyte adhesiveness, in patients with hypercholesterolaemia. Int J Exp Pathol 78,259-66. 

Risk and protective factors of atherosclerosis influence VCAM-1 expression [10,19]. A possible relation between VC AM expression and oxidized LDL was established when an important component of this modified lipoprotein, lysophosphatidylcholine, was shown to stimulate VCAM expression and increase adhesion of monocytes on endothelium in cell cultures [10,18,19]. Modified LDL and its constituents augment c)4 okine-activated VCAM-1 expression in human vascular endothelial cells [10,20]. In contrast, HDL inhibits cytokine-induced expression of endothelial cell adhesion molecules [10,21]. -3 Fatty acids have been found to decrease mRNA levels and surface expression of VCAM-1 in endothelial cells [10,22]. Aspirin inhibits induction of mRNA and cell surface expression of VCAM-1 by TNF-a and thereby inhibits monocyte adhesion on stimulated endothelial cells [10,23]. In contrast to ICAM-1, E-selectin, and P-selectin, endothelial VCAM-1 can mediate leukocyte adhesion via its sole interaction with the integrins 4P1 or 4P7 [10]. 

C. Weber, W. Erl, A. Pietsch and P. Weber, Aspirin Inhibits Nuclear Factor-B Mobiliiation and Monocyte Adhesion in Stimulated Human Endothelial Cells, Circulation 9i (1995) 1914-1917. 

Bolick, D. T., Srinivasan, S., Kim, K. W., Hatley, M. E., Clemens, J. J., Whetzel, A., Eerger, N., Macdonald, T. L., Davis, M. D., Tsao, P. S., Lynch, K. R., Hedrick, C. C. Sphingo-sine-1-phosphate prevents tumor necrosis factor- alpha -mediated monocyte adhesion to aortic endothelium in mice. Arterioscler Thromb Vase Biol 25 (2005) 976-981. 

Huber, J. et al. Specific monocyte adhesion to endothelial cells induced by oxidized phospholipids involves activation of cPLA2 and lipoxygenase. J. Lipid Res. 47 (2006) 1054-62. 

Another fate of arachidonic acid with potential relevance to atherosclerosis is cytochrome P450 monooxygenase-derived metabolism to epoxyeicosatrienoic acids (EETs) (Chapter 12), which may also be formed non-enzymatically by the interaction of arachidonic acid with free radicals (D.D. Gutterman, 2006). EET synthesis in cultured endothelial cells can be induced by LDL, and EETs are found both in LDL and in human atherosclerotic lesions. Biological effects of EETs include potentially anti-atherogenic effects, such as vasodilatation and prevention of platelet aggregation, and atherogenic responses, such as increased monocyte adhesion. 

Dietary intake of n-6 fatty acids such as linoleic acid, and n-3 fatty acids, such as the fish oils eicosapentanoic acid and docosahexaenoic acid, lowers plasma cholesterol and antagonizes platelet activation, but the fish oils are much more potent in this regard [26]. In particular, n-3 fatty acids competitively inhibit thromboxane synthesis in platelets but not prostacyclin synthesis in endothelial cells. These fatty acids have also been shown to have other potentially anti-atherogenic effects, such as inhibition of monocyte cytokine synthesis, smooth muscle cell proliferation, and monocyte adhesion to endothelial cells. While dietary intake of n-3 fatty acid-rich fish oils appears to be atheroprotective, human and animal dietary studies with the n-6 fatty acid linoleic acid have yielded conflicting results in terms of effects on both plasma lipoproteins and atherosclerosis. Indeed, excess amounts of both n-3 and n-6 fatty acids may actually promote oxidation, inflammation, and possibly atherogenesis (M. Toberek, 1998). In this context, enzymatic and non-enzymatic oxidation of linoleic acid in the sn-2 position of LDL phospholipids to 9- and 13-hydroxy derivatives is a key event in LDL oxidation (Section 6.2). 

In vitro experiments demonstrated an anti-inflammatory effect of soy isoflavones, including inhibition of monocyte adhesion to vascular endothelial cells (Chacko et al.,... 

McNally, A.K. and J.M. Anderson, Complement C3 participation in monocyte adhesion to different surfaces. Proceedings of the National Academy of Sciences USA, 1994, 91, 10119-10123.. 

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