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Senescence marker protein 30 is up‐regulated in kainate‐induced hippocampal damage through ERK‐mediated astrocytosis
Author(s) -
Son Tae Gen,
Park Hee Ra,
Kim So Jung,
Kim Keunho,
Kim MinSun,
Ishigami Akihito,
Handa Setsuko,
Maruyama Naoki,
Chung Hae Young,
Lee Jaewon
Publication year - 2009
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.22122
Subject(s) - astrocytosis , senescence , hippocampal formation , kainate receptor , mapk/erk pathway , microbiology and biotechnology , neuroscience , chemistry , biology , phosphorylation , biochemistry , glutamate receptor , central nervous system , ampa receptor , receptor
Abstract Senescence maker protein 30 (SMP30) is decreased in an androgen‐independent manner in kidney and liver with age. However, regulation of SMP30 expression in the brain has not been examined in aging and neurodegenerative diseases. To investigate SMP30 expression in the brain, we utilized aging and kainate (KA)‐induced neurodegenerative disease models. Interestingly, expression of SMP30 was unlikely to decrease in the aged brain, but total levels of SMP30 protein were increased at 4 weeks after KA injury. Increased glial fibrillary acidic protein (GFAP) with elevated SMP30 expression was observed at the same time post‐KA, indicating that regulation of SMP30 expression in the brain may be associated with astrocytosis. We confirmed that KA induced GFAP expression with increased SMP30 in rat astrocyte cells. Moreover, we found that ERK1/2 activation was involved in the up‐regulation of SMP30 in astrocytes. Our results suggest that elevated SMP30 in activated astrocytes plays an important supportive role after brain damage. © 2009 Wiley‐Liss, Inc.