Research ArticleNeuroscience

STIM2 Regulates Capacitive Ca2+ Entry in Neurons and Plays a Key Role in Hypoxic Neuronal Cell Death

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Science Signaling  20 Oct 2009:
Vol. 2, Issue 93, pp. ra67
DOI: 10.1126/scisignal.2000522

Resisting Ischemia

Loss of blood flow to the brain—as can occur during a stroke—leads to the death of neurons, a process that involves a pathological increase in intracellular calcium. Berna-Erro et al. investigated the role of capacitive calcium entry (CCE), a process in which depletion of calcium from intracellular stores triggers its entry across the plasma membrane, in ischemia-induced calcium entry and neuronal death. The calcium-sensing molecule STIM1 is known to play a crucial role in mediating CCE in various cell types; in neurons, however, Berna-Erro et al. found that CCE depended instead on the closely related molecule STIM2. Neurons from mice lacking STIM2 were resistant to the effects of hypoxia in vitro; moreover, mice lacking STIM2 showed less neurological damage than did wild-type mice in a model of ischemic stroke. Thus, the authors conclude that STIM2 is critical to neuronal CCE and that CCE plays a role in neuronal death in ischemia.

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