The synthesis of glial-fibrillary acidic protein (GFAP) or the re-expression of progenitor markers such as Nestin increases in reactive astrocytes after brain ischemia. We investigated the dynamics of reactive astrocytes after transient focal brain ischemia by examining the expression of Musashi1 (Msi1), an RNA-binding protein and another marker of neural stem/progenitor cells. In ischemic striatum induced by middle cerebral artery occlusion (MCAO), an increase in Msi1-immunoreactivity was observed from 2 days after MCAO, persisting until 14 days. The proliferation of Msi1-positive cells was observed from 4 days after MCAO and reached a peak at 7 days. These Msi1-positive cells were regarded as reactive astrocytes based on their co-expression with GFAP or Nestin and their morphology. Msi1-positive cells were located in the peri-infarct area in a region similar, but not identical, to that of Nestin-positive cells. The Msi1+Nestin+ cells were located much closer to the ischemic core than the Msi1+Nestin- cells. The present study revealed that Msi1-expression, similar to Nestin, is induced after brain ischemia and may be involved in the reactivation of astrocytes, including their proliferation. However, the difference in the distributions of Msi1 and Nestin suggests that some of their features may differ in reactive astrocytes.
- Brain ischemia
- Glial-fibrillary acidic protein (GFAP)
- Middle cerebral artery occlusion (MCAO)
- Musashi1 (Msi1)
- Reactive astrocyte
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