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vß3)1
Departments of
*
Medicine and
Pediatrics, National Jewish Medical and Research Center, and
Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262
In vivo, apoptotic cells are efficiently removed by professional or
nonprofessional phagocytes, a process thought to be essential for
tissue remodeling and resolution of inflammation. Macrophages recognize
apoptotic cells by several mechanisms, including recognition of exposed
phosphatidylserine (PS); however, PS recognition on apoptotic cells has
not been identified as a feature of human macrophages. The purpose of
this study was to determine whether human monocyte-derived macrophages
could be stimulated to recognize PS, defined as inhibition of
phagocytosis by PS-containing liposomes. We also assessed the potential
roles for scavenger receptors, CD14, and lectins. Uptake of apoptotic
neutrophils into unstimulated macrophages was blocked about 50% by
Arg-Gly-Asp-Ser and anti-
v, and up to 20% by
oxidized low density lipoprotein and
N-acetylglucosamine, implying a major role for integrin
and minor roles for scavenger and lectin receptors. Uptake into
macrophages stimulated with ß-1,3-glucan was blocked 50% by PS
liposomes and 40% by oxidized low density lipoprotein, suggesting that
the macrophages had switched from using integrin to recognition of PS.
MEM-18 and 61D3 (anti-CD14 mAbs) were poor inhibitors of apoptotic
neutrophil uptake, but good inhibitors of apoptotic lymphocyte uptake.
The switch to PS recognition was accompanied by down-regulation of
vß3 expression and function. Anti-CD36
blocked uptake into unstimulated or stimulated macrophages, suggesting
CD36 involvement not only with the vß3
integrin mechanism (as previously reported) but also with PS
recognition. A maximum of 70% inhibition was achieved by combining
anti-CD36 with either anti-av or PS
liposomes.
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M.-K. Chang, C. Bergmark, A. Laurila, S. Horkko, K.-H. Han, P. Friedman, E. A. Dennis, and J. L. Witztum Monoclonal antibodies against oxidized low-density lipoprotein bind to apoptotic cells and inhibit their phagocytosis by elicited macrophages: Evidence that oxidation-specific epitopes mediate macrophage recognition PNAS, May 25, 1999; 96(11): 6353 - 6358. [Abstract] [Full Text] [PDF]
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S. C. Frasch, P. M. Henson, J. M. Kailey, D. A. Richter, M. S. Janes, V. A. Fadok, and D. L. Bratton Regulation of Phospholipid Scramblase Activity during Apoptosis and Cell Activation by Protein Kinase Cdelta J. Biol. Chem., July 21, 2000; 275(30): 23065 - 23073. [Abstract] [Full Text] [PDF]
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V. A. Fadok, A. de Cathelineau, D. L. Daleke, P. M. Henson, and D. L. Bratton Loss of Phospholipid Asymmetry and Surface Exposure of Phosphatidylserine Is Required for Phagocytosis of Apoptotic Cells by Macrophages and Fibroblasts J. Biol. Chem., January 5, 2001; 276(2): 1071 - 1077. [Abstract] [Full Text] [PDF]
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R. F. Thorne, J. F. Marshall, D. R. Shafren, P. G. Gibson, I. R. Hart, and G. F. Burns The Integrins alpha 3beta 1 and alpha 6beta 1 Physically and Functionally Associate with CD36 in Human Melanoma Cells. REQUIREMENT FOR THE EXTRACELLULAR DOMAIN OF CD36 J. Biol. Chem., November 3, 2000; 275(45): 35264 - 35275. [Abstract] [Full Text] [PDF]
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T. Miyahara, L. Schrum, R. Rippe, S. Xiong, H. F. Yee Jr., K. Motomura, F. A. Anania, T. M. Willson, and H. Tsukamoto Peroxisome Proliferator-activated Receptors and Hepatic Stellate Cell Activation J. Biol. Chem., November 10, 2000; 275(46): 35715 - 35722. [Abstract] [Full Text] [PDF]
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