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First published online January 23, 2008

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Death by shrinkage

Cell condensation is a hallmark of apoptosis. This decrease in volume – which occurs during both the intrinsic and extrinsic apoptotic pathways – is thought to result from the efflux of chloride ions, and subsequently water, from the cell. The importance of cell condensation in the apoptotic program remains unclear – is it a by-product of other processes, or a necessary step on the path to apoptosis? On page 290, Harald Sontheimer and colleagues explore mechanisms of cell condensation in human glioma cells. The authors show that DIDS, an inhibitor of chloride channels, stops cells from shrinking and consequently blocks apoptosis by either pathway. The authors go on to show that glioma cells can be induced to shrink by hyperosmotic shock; importantly, this shrinkage triggers apoptosis, even without additional death stimuli. The authors propose that cell condensation might trigger apoptosis by bringing auto-activating enzymes and cell-surface receptors into closer proximity. These results identify cell condensation as a key effector step in apoptosis.

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Related articles in JCS:

Cytoplasmic condensation is both necessary and sufficient to induce apoptotic cell death

Nola Jean Ernest, Christa W. Habela, and Harald Sontheimer
JCS 2008 121: 290-297. [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?