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Monocyte-derived macrophage

Yeh MW, Kaul M, Zheng J, Nottet HS, Thylin M, Gendelman HE, Lipton SA (2000) Cytokine-stimulated, but not HIV-infected, human monocyte-derived macrophages produce neurotoxic levels of 1 -cysteine. J Immunol 164(8) 4265-4270... [Pg.32]

Byrn RA, Kiesshng AA (1998) Analysis of human immunodeficiency virus in semen indications of a genetically distinct virus reservoir. J Reprod Immunol 41(1-2) 161-176 Carr JM, Hocking H, Li P, Burrell CJ (1999) Rapid and efficient celL-to-ceU transmission of human immunodeficiency vims infection from monocyte-derived macrophages to peripheral blood lymphocytes. Virology 265(2) 319-329... [Pg.109]

Perhaps most importantly, MOP agonists can potentiate HIV propagation in lymphocytes, monocytes, and monocyte-derived macrophages/microglia (Peterson et al. 1990 Carr and Serou 1995). This includes morphine (Peterson et al. 1990, 1999, 2004 Hu et al. 2005), methadone (Douglas 2001), and the MOP peptide agonist endomorphin (Peterson et al. 1999). The effects of morphine on HIV... [Pg.358]

Dysfunction of the endothelium allows lipoproteins, predominantly low-density lipoprotein (LDL) cholesterol, and inflammatory cells, namely monocytes and T lymphocytes, to migrate from the plasma to the sub-endothelial space. Monocyte-derived macrophages ingest lipoproteins to form foam cells. Macrophages also secrete growth factors that promote smooth muscle cell migration from the media to the intima. A fatty streak consists of lipid-laden macrophages and smooth muscle cells and is the earliest type of atherosclerotic lesion. [Pg.66]

Von Eckardstein, A, Langer, C, Engel, T, Schaukal, I, Cignarella, A, Reinhardt, J, Lorkowski, S, Li, Z, Zhou, X, Cullen, P, and Assmann, G, 2001. ATP binding cassette transporter ABCA1 modulates the secretion of apolipoprotein E from human monocyte-derived macrophages. FASEB J 15, 1555-1561. [Pg.353]

It was found that the HIV envelope glycoprotein in vitro increases the production of NO by human monocyte-derived macrophages [114]. NO production is increased in patients who have AIDS [115], and the increased concentrations of nitrite in AIDS patients with opportunistic infections is caused by T gondii, Pneumocystis carinii, Mycobacterium tuberculosis, and Mycobacterium avium, whereas nitrite concentrations are normal in symptom-free patients. It was also confirmed that there was increased production of NO in the sera of children with HIV-1 infection, and of circulating cytokines, such as interleukin lp, tumor necrosis factor a, and interferon y. It is postulated that rises in the concentrations of these cytokines may represent a substantial stimulation of NO production [116]. In contrast, it has been shown that there was no altered endogenous nitrate formation in eight patients with AIDS, most of whom had opportunistic infections [117]. It has also been noted that there were high... [Pg.20]

These observations were taken further by examining whether y-interferon treatment could up-regulate NADPH oxidase function in CGD neutrophils and monocytes. It was found that 12 out of 13 patients with autosomal recessive CGD had increased oxidase activity upon y-interferon exposure the only patient not responding was the one devoid of the b cytochrome. In X-linked CGD, 9 of 13 showed no improvement, whereas 3 showed some improvement and 1 had oxidase activity increased to near-normal levels. Patients with atypical X-linked CGD (i.e. low oxidase activity and some cytochrome b) appear to respond best to y-interferon treatment. Interferons-a and -ft are without affect. This enhancement of oxidase function (detected by NBT slide tests and O2 production) is due, at least in part, to increased levels of mRNA for the heavy chain of cytochrome b. In the absence of y-interferon treatment, monocyte-derived macrophages have extremely low or undetectable levels of mRNA for the cytochrome b heavy chain however, this is increased about fivefold (to about 5% of normal) after y-interferon treatment. [Pg.271]

Snijder, M. L., Polacek, D., Scanu. A. M., and Fless, G. M., Comparative binding and degradation of lipoprotein(a) and low density lipoprotein by human monocyte-derived macrophages. J. Biol. Chem. 267, 339-346 (1992). [Pg.131]

Porter AE, Gass M, Muller K, Skepper JN, Midgley P, Welland M (2007) Visualizing the uptake of C60 to the cytoplasm and nucleus of human monocyte-derived macrophage cells using energy-filtered transmission electron microscopy and electron tomography. Environ. Sci. Technol. 41 3012-3017. [Pg.20]

Nicholson, A.C., Friede, S., Pearce, A., and SUverstein, R.L., 1995, Oxidized LDL binds to CD36 on human monocyte-derived macrophages and transfected ceU Unes Evidence implicating the lipid moiety of the lipoprotein as the binding Aie.,Arterioscl. Tromb. Vase. Biol. 15 269-275. [Pg.94]

Anthonsen, M.W., Stengel, D., Hourton, D., Ninio, E., Johansen, B., 2000, Mildly oxidized LDL induces expression of group 11a secretory phospholipase A(2) in human monocyte-derived macrophages, Arterioscler Thromb Vase Biol, 20 1276-1282. [Pg.141]

Asmis, R., Wintergerst, E.S., 1998, Dehydroascorbic add prevents apoptosis induced by oxidized low-density lipoprotein in human monocyte-derived macrophages, Eur. J. Biochem. 255 147-155. [Pg.141]

Janabi, M., Yamashita, S., Hirano, K., Sakai, N., Hiraoka, H., Matsumoto, K., Zhang, Z., Nozaki, S., and Matsuzawa, Y., 2000, Oxidized LDL-induced NF-kappa B activation and subsequent expression of proinflammatory genes are defective in monocyte-derived macrophages from CD36-deficient patients, Arteriosc/er. Thromb. Vase. Biol. 20 1953-1960. [Pg.145]

Heredia A, Davis C, Redfield R. 2000. Synergistic inhibition of HIV-1 in activated and resting peripheral blood mononuclear cells, monocyte-derived macrophages, and... [Pg.323]

Erbacher, P., Bousser, M.-T., Raimond, J., Monsigny, M., Midoux, P. and Roche, A.C. (1996b) Gene transfer by DNA/ glycosylated polylysine complexes into human blood monocyte-derived macrophages. Hum. Gene Ther., 7, 721-729. [Pg.331]

K. Hirano, S. Yamashita, Y. Nakagawa, T. Ohya, F. Matsuura, T. Tsukamoto, Y. Okamoto, A. Matsuyama, K. Matsumoto, J. Miyagawa and Y. Matsuzawa, Expression of human scavenger receptor class B type I in cultured human monocyte-derived macrophages and atherosclerotic lesions, Circ. Res. 85 (1999) 108-116. [Pg.315]

We have demonstrated that human monocyte derived macrophages (HMDMs) isolated from NIDDM patients after consumption of PJ for 3 months, the carotid lesion derived after endartherectomy from CAS patients that consumed PJ (Figure 8.4A), and also mouse peritoneal macrophages (MPMs) isolated from E° mice after consumption of PJ concentrate (12.5 pL/mouse/day, equivalent to 0.35 pmol of total... [Pg.144]

Ammon C, Meyer SP, Schwarzfischer L, Krause SW, Andreesen R, Kreutz M. Comparative analysis of integrin expression on monocyte-derived macrophages and monocyte-derived dendritic cells. Immunology 2000, 100, 364—369. [Pg.52]

H8. Herrmann, M., Voll, R. E., Zoller, O. M., Hagenhofer, M., Ponner, B. B., and Kalden, J. R., Impaired phagocytosis of apoptotic cell material by monocyte-derived macrophages from patients with systemic lupus erythematosus. Arthritis Rheum. 41, 1241-1250 (1998). [Pg.162]

C6. Chait, A., Iverius, P.-H., and Brunzell, J. D., Lipoprotein lipase secretion by human monocyte-derived macrophages. J. Clin. Invest. 69, 490—493 (1982). [Pg.272]

Atherosclerosis is a complex disease, characterized by an excessive inflammatory, fibro-fatty, proliferative response to damage of the artery wall involving several cell types, particularly smooth muscle cells, monocyte-derived macrophages, T-lymphocytes and platelets (Schwartz et al., 1993). [Pg.322]


See other pages where Monocyte-derived macrophage is mentioned: [Pg.186]    [Pg.96]    [Pg.110]    [Pg.239]    [Pg.331]    [Pg.354]    [Pg.355]    [Pg.358]    [Pg.367]    [Pg.191]    [Pg.255]    [Pg.794]    [Pg.794]    [Pg.21]    [Pg.95]    [Pg.282]    [Pg.174]    [Pg.795]    [Pg.795]    [Pg.576]    [Pg.14]    [Pg.21]    [Pg.35]    [Pg.139]    [Pg.38]    [Pg.234]   
See also in sourсe #XX -- [ Pg.109 ]




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Monocytes monocytic

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