The p38 MAPK signaling pathway has been implicated in various pathological conditions of neuronal and non-neuronal cells. Here we report the differential induction of p38 MAPK isoforms, p38α and p38β, in the adult gerbil brain following transient global ischemia. The p38α and p38β kinase activities were gradually enhanced with the peak activity occurring around 2-4 days after ischemic insult. Immunohistochemical analysis revealed that p38α expression was increased as early as 4 h after ischemic insult and enhanced further reaching maximum induction around 4 days after ischemia. The induced p38α was concentrated in microglia in hippocampus as well as in frontal and parietal cortices of the brain, where significant neuronal damage was occurred. By contrast, immunostaining with anti-p38β antibody indicated that p38β was markedly induced in astrocytes in hippocampus around 4 days after ischemic insult, which lasted for the next several days. The differential induction of p38 MAPK isoforms following transient global ischemia, especially the induction of p38α and p38β MAPKs in microglia and astrocytes, respectively, in different time points after ischemic insult suggest distinct roles of p38 MAPK isoforms in post-ischemic brain.
- Global ischemia
- p38 MAPK
ASJC Scopus subject areas
- Molecular Biology
- Cellular and Molecular Neuroscience