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Apoptosis vs necrosis: ceramide decides it

Cells that apoptose yield vesicles without releasing their content. Death by necrosis, by contrast, involves cell swelling and lysis and can therefore generate inflammatory responses. But what determines whether a cell undergoes apoptosis or necrosis? Andrew Quest and co-workers have approached this question by examining Fas-induced death of A20 B lymphoma cells (see p. 4671). They observe that — as expected — Fas ligand triggers apoptosis, and this is accompanied by and dependent on activation of caspase-8 (the initiator caspase recruited to the Fas death receptor) and caspase-3 (a downstream effector caspase). Interestingly, apoptosis only occurs in 60% of cells. The rest undergo necrosis, and this requires caspase-8 but not caspase-3. The authors also observe that death of A20 cells is accompanied by ceramide generation, which, like necrosis, requires caspase-8 but not caspase-3. Furthermore, they demonstrate that ceramide treatment can promote necrosis of lymphoid cells and that a lymphoid line that does not generate ceramide undergoes Fas-induced apoptosis but not necrosis. Ceramide thus seems to determine how the cells die, which could be important given that necrosis is critical for certain immune responses.

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Caspase-dependent initiation of apoptosis and necrosis by the Fas receptor in lymphoid cells: onset of necrosis is associated with delayed ceramide increase

Claudio A. Hetz, Martin Hunn, Patricio Rojas, Vicente Torres, Lisette Leyton, and Andrew F. G. Quest
JCS 2002 115: 4671-4683. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?