AI Article Synopsis
- O-GlcNAcylation is a significant modification that affects nucleocytoplasmic proteins and plays a role in various biological processes, particularly during cerebral ischemia.
- Researchers found that O-GlcNAcylation levels increased shortly after ischemia and then declined, with a moderate increase improving outcomes for brain injuries caused by lack of blood flow.
- The study suggests that enhancing O-GlcNAcylation could be a potential treatment strategy to mitigate damage from ischemic strokes, as indicated by similar changes observed in postmortem human brain tissues.
Article Abstract
O-GlcNAcylation is a common posttranslational modification of nucleocytoplasmic proteins with β-N-acetylglucosamine (GlcNAc) and regulates numerous biological processes. By using mouse models of cerebral ischemia induced by permanent and transient middle cerebral artery occlusion (MCAO), we observed an initial elevation (~1.7-fold, 1-4 hours after ischemia) and then decline of O-GlcNAcylation during cerebral ischemia. We found that moderate increase (<3-fold) of brain O-GlcNAcylation by pharmacological means ameliorated cerebral ischemia-reperfusion injury and the consequent motor and neurological deficits. Interference of the transient elevation of O-GlcNAcylation pharmacologically or genetically aggravates the ischemia-induced brain damage, motor deficits and mortality. The alteration of O-GlcNAcylation was also seen in the ischemic areas of postmortem human brains. This study reveals an important regulation of cerebral ischemia-reperfusion injury by O-GlcNAcylation and also provides a possible therapeutic strategy, i.e., by increasing O-GlcNAcylation, to reduce the cerebral damage and improve the clinical outcome of ischemic stroke.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5587588 | PMC |
| http://dx.doi.org/10.1038/s41598-017-10635-0 | DOI Listing |
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