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Activation of p38 MAPK in Microglia After Ischemia
Author(s) -
Walton Kevin M.,
DiRocco Richard,
Bartlett Becky A.,
Koury Elizabeth,
Marcy Val Robert,
Jarvis Bruce,
Schaefer Erik M.,
Bhat Ratan V.
Publication year - 1998
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1998.70041764.x
Subject(s) - microglia , p38 mitogen activated protein kinases , neurodegeneration , ischemia , protein kinase a , phosphorylation , hippocampus , mitogen activated protein kinase , forebrain , mapk/erk pathway , proinflammatory cytokine , microbiology and biotechnology , kinase , endocrinology , medicine , neuroscience , chemistry , biology , inflammation , central nervous system , disease
p38 MAPK has been implicated in the regulation of proinflammatory cytokines and apoptosis in vitro. To understand its role in neurodegeneration, we determined the time course and localization of the dually phosphorylated active form of p38 MAPK in hippocampus after global forebrain ischemia. Phosphorylated p38 MAPK and mitogen‐activated protein kinase‐activated protein 2 activity increased over 4 days after ischemia. Phosphorylated p38 MAPK immunoreactivity was observed in microglia in regions adjacent to, but not in, the dying CA1 neurons. In contrast, neither c‐Jun N‐terminal kinase 1 nor p42/p44 MAPK activity was altered after ischemia. These results provide the first evidence for localization of activated p38 MAPK in the CNS and support a role for p38 MAPK in the microglial response to stress.