© 2000 by Society
© 2000 by the Society forNeuro-Oncology
Phosphatidylserine-dependent phagocytosis of apoptotic glioma cells bynormal human microglia, astrocytes, and glioma cells
Department of Neurosurgery, University of California at SanFrancisco, San Francisco, CA 94115
1 Address correspondence and reprint requests to Russell O. Pieper, Universityof California at San Francisco, Department of Neurosurgery and The Brain TumorResearch Center, 2340 Sutter St., Rm. N261-Box 0128, San Francisco, CA 94115.
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Abstract |
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Apoptotic cells display signals that trigger phagocytic removal bymacrophages or neighboring cells. To better understand the signals triggeringphagocytosis of apoptotic glioma cells, and to identify the cells that mightbe involved in the phagocytic process, U-251 MG glioma cells were madeapoptotic by etoposide (25 µg/ml) treatment and were incubated with normalhuman astrocytes (NHA), glioma cells, or microglia. Extent of phagocytosis wasassessed by an in vitro phagocytosis assay. After 3 h of incubation withapoptotic cells, phagocytes tested were washed to remove nonengulfed cells,then fixed, stained, and counted to determine phagocytosis index (PI). NHA,glioma cells, and microglia all phagocytosed apoptotic, but not nonapoptotic,glioma cells. Microglia, however, had a PI approximately 4-fold higher thandid either NHA or glioma cells. Binding of phosphatidylserine (PS) onapoptotic glioma cell membranes by annexin-V inhibited phagocytosis by 90% inboth microglia and NHA. The activity of an enzyme (scramblase) that moves PSfrom the inner cell membrane to the outer cell membrane was also increased inapoptotic glioma cells. These results suggest that a variety of cells presentin and near gliomas in vivo can remove glioma cells in a PS-dependentscramblase-mediated fashion. Manipulation of scramblase and/or PS exposure inglioma cells may therefore be a means of triggering phagocytic removal ofglioma cells.
Received March 3, 2000; Accepted April 18, 2000
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