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• W2576278996 abstract "We recently demonstrated that ischemic tolerance was dependent on astrocytes, for which HIF‐1α had an essential role. The mild ischemia (preconditioning; PC) increased HIF‐1α in a biphasic pattern, that is, a quick and transient increase in neurons, followed by a slow and sustained increase in astrocytes. However, mechanisms underlying such temporal difference in HIF‐1α increase remain totally unknown. Here, we show that unlike a hypoxia‐dependent mechanism in neurons, astrocytes increase HIF‐1α via a novel hypoxia‐independent but P2X7‐dependent mechanism. Using a middle cerebral artery occlusion (MCAO) model of mice, we found that the PC (a 15‐min MCAO period)‐evoked increase in HIF‐1α in neurons was quick and transient (from 1 to 3 days after PC), but that in astrocytes was slow‐onset and long‐lasting (from 3 days to at least 2 weeks after PC). The neuronal HIF‐1α increase was dependent on inhibition of PHD2, an oxygen‐dependent HIF‐1α degrading enzyme, whereas astrocytic one was independent of PHD2. Astrocytes even do not possess this enzyme. Instead, they produced a sustained increase in P2X7 receptors, activation of which resulted in HIF‐1α increase. The hypoxia‐independent but P2X7‐receptor‐dependent mechanism could allow astrocytes to cause long‐lasting HIF‐1α expression, thereby leading to induction of ischemic tolerance efficiently. GLIA 2017;65:523–530" @default.
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• W2576278996 date "2017-01-07" @default.
• W2576278996 modified "2023-10-05" @default.
• W2576278996 title "Hypoxia‐independent mechanisms of HIF‐1α expression in astrocytes after ischemic preconditioning" @default.
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• W2576278996 doi "https://doi.org/10.1002/glia.23109" @default.
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