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- W1991854893 abstract "Researchers suggest that endoplasmic reticulum (ER) stress cause apoptosis after ischemia. Caspase-12 has been localized to the ER and is a signal for apoptosis. We sought to clarify the role of caspase-12 in the vascular endothelial growth factor (VEGF) induced neuroprotective effect. Transient focal cerebral ischemia was produced by occluding left middle cerebral artery in rabbit. The expressions of caspase-12 and caspase-3 were detected by immunohistochemistry. Neuronal apoptosis was detected by TUNEL staining. We confirmed that the number of apoptotic cells and the expressions of caspase-12 and caspase-3 significantly increased during reperfusion. VEGF inhibited the cell apoptosis and the expressions of caspase-12 and caspase-3. These results suggest that VEGF may protect neurons from apoptosis by inhibiting ER stress pathway." @default.
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- W1991854893 date "2009-01-01" @default.
- W1991854893 modified "2023-09-27" @default.
- W1991854893 title "Effect of Endoplasmic Reticulum Stress in VEGF-Induced Neuroprotection" @default.
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- W1991854893 doi "https://doi.org/10.1080/08941930802566714" @default.
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