Published online March 12, 2007
doi:10.1083/jcb.1766iti5
The Journal of Cell Biology, Vol. 176, No. 6, 731b-
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Leslie
Die another way
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The characteristic signs of necrosis (top) are missing in a neuron dosed with ProT (bottom).
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On page 853 Ueda et al. describe a protein that switches cells between two death mechanisms, preventing necrosis while promoting apoptosis. The molecule might provide a new way to save brain cells after a stroke.
A stroke delivers a double whammy. First, cells near the clot begin to perish from necrosis, which is triggered by ATP scarcity. Later, more distant cells start dying through apoptosis. Although anti-apoptosis compounds can stem some damage, their benefits are modest, possibly because the necrosis is more devastating. Molecules to halt necrosis have proven elusive.
Ueda et al. found one such molecule in cultures of rat cortical neurons. The protein ProT curbs necrosis in cultures that lack serum or have been oxygen deprived. But it also boosts their apoptotic death rates. Adding growth factors that derail apoptosis protects most of the cells.
The group showed that ProT works by keeping cells well-nourished. During necrosis, some of the GLUT transporters that usher glucose into the cell exit the plasma membrane. But ProT prevents this relocation.
Ueda et al. conclude that ProT flips cells from an uncontrollable form of cell death, necrosis, to a more controllable one. Other factors can derail cells from apoptosis. A treatment that mixes ProT with some of these compounds might spare neurons after a stroke. 
Mitch Leslie
mitchleslie{at}comcast.net
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