Recent studies have suggested that
nestin facilitates cellular structural remodeling in vasculature-associated cells in response to ischemic injury. The current study was designed to investigate the potential role of post-ischemic
nestin expression in parenchymal astrocytes. With this aim, we characterized
ischemia-induced
nestin expression in the CA1 hippocampal region, an area that undergoes a delayed neuronal death, followed by a lack of neuronal generation after transient forebrain
ischemia. Virtually all of the
nestin-positive cells in the ischemic CA1 hippocampus were reactive astrocytes. However, induction of
nestin expression did not correlate simply with
astrogliosis, but rather showed characteristic time- and strata-dependent expression patterns.
Nestin induction in astrocytes of the pyramidal cell layer was rapid and transient, while a long-lasting induction of
nestin was observed in astrocytes located in the CA1 dendritic subfields, such as the stratum oriens and radiatum, until at least day 28 after
ischemia. There was no detectable expression in the stratum lacunosum moleculare despite the evident astroglial reaction. Almost all of the
nestin-positive cells also expressed a
transcription factor for neural/glial progenitors, i.e., Sox-2 or Sox-9, and some cells were also positive for Ki-67. However, all of the
nestin-positive astrocytes expressed the
calcium-binding protein S100β, which is known to be expressed in a distinct, post-mitotic astrocyte population. Thus, our data indicate that in the ischemic CA1 hippocampus,
nestin expression was induced in astroglia that were becoming reactive, but not in a progenitor/stem cell population, suggesting that
nestin may allow for the structural remodeling of these cells in response to ischemic injury.