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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We used proteomics to identify regulated proteins following cerebral ischemia in a rat model. Young rats were subjected to reversible middle cerebral artery (MCA) occlusion and proteins were extracted from the peri-infarcted and the corresponding contralateral area at days 3 and 14 postischemia. Proteins were analyzed by two-dimensional polyacrylamide gel electrophoresis followed by mass spectrometry. We report for the first time that an isoform of annexin A3 (ANXA3) was among the upregulated proteins in the postischemic rat brain. The results were confirmed by real-time PCR and by western blotting. Double- and triple-immunostaining with neuronal and microglia/macrophagic markers demonstrated that ANXA3 is produced by resting microglia in control tissue and by activated microglial/macrophage cells in the infarcted area. 3D-images of the infarcted area suggest that ANXA3 is associated with a phagocytic phenotype. Our study identifies ANXA3 as a novel marker of brain microglia, which should be of substantial value in future studies of microglial cells and its role in the postischemic brain.
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PMID:Proteomic identification of an upregulated isoform of annexin A3 in the rat brain following reversible cerebral ischemia. 1782 64

In an effort to identify new proteins involved in functional recovery after cerebral ischemia, young (3 months) and aged (18 months) male rats were subjected to middle cerebral artery (MCA) occlusion. Brains were harvested at 3- and 14-days post ischemia and proteins from the peri-infarcted and the corresponding contralateral area and total proteins were analyzed by two-dimensional polyacrylamide gel electrophoresis followed by mass spectrometry analysis. Annexin A3 (ANXA3) was identified as one upregulated protein in the post-ischemic rat brain. Using western blotting, real-time PCR and immunohistochemistry, we confirmed that at 3-14 days post-stroke, ANXA3 expression in the peri-infarct area was consistently increased over the corresponding area of control rats. Double staining revealed that ANXA3 is produced by activated microglial cells. We found that aged rats also had more newly proliferating cells expressing ANXA3 than young rats do. Occasionally, ANXA3-immunopositive cells wraped around neurons, suggesting that annexin A3 may be involved in the removal of dying neurons after stroke.
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PMID:Annexin A3 expression after stroke in the aged rat brain. 1827 99