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Region-specific changes in aquaporin 4 induced by hyperglycemia underlie the differences in cell swelling in the cortex and striatum after cerebral ischemia-reperfusion
•AQP4 immunoreactive intensity differences in the cortical and striatal penumbra were assessed.•Hyperglycemia had more serious effects on striatal penumbra after ischemia.•Hyperglycemia induced more serious brain edema on striatal penumbra after ischemia.•These findings may explain the role of diabe...
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Published in: | Neuroscience letters 2021-05, Vol.754, p.135885-135885, Article 135885 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | •AQP4 immunoreactive intensity differences in the cortical and striatal penumbra were assessed.•Hyperglycemia had more serious effects on striatal penumbra after ischemia.•Hyperglycemia induced more serious brain edema on striatal penumbra after ischemia.•These findings may explain the role of diabetes in cerebral ischemic injury.
Brain edema is a major cause of death in patients who suffer an ischemic stroke. Diabetes has been shown to aggravate brain edema after cerebral ischemia-reperfusion, but few studies have focused on the heterogeneity of this response across different brain regions. Aquaporin 4 plays an important role in the formation and regression of brain edema. Here, we report that hyperglycemia mainly affects the continuity of aquaporin 4 distribution around blood vessels in the cortical penumbra after ischemia-reperfusion; however, in the striatal penumbra, in addition to affecting the continuity of distribution, it also substantially affects the fluorescence intensity and the polarity distribution in astrocytes. Accordingly, hyperglycemia induces a more significant increase in the number of swelling cells in the striatal penumbra than in the cortical penumbra. These results can improve our understanding of the mechanism underlying the effects of diabetes in cerebral ischemic injury and provide a theoretical foundation for identification of appropriate therapeutic modalities. |
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ISSN: | 0304-3940 1872-7972 |
DOI: | 10.1016/j.neulet.2021.135885 |