> Details

Son, Tae Gen; Park, Hee Ra; Kim, So Jung; Kim, Keunho; Kim, Min‐Sun; Ishigami, Akihito; Handa, Setsuko; Maruyama, Naoki; Chung, Hae Young; Lee, Jaewon

Senescence marker protein 30 is up‐regulated in kainate‐induced hippocampal damage through ERK‐mediated astrocytosis

Reference
management

Bookmarks

Remove from
bookmarks

Share this on Whatsapp

Close

Bookmarks



You can manage bookmarks using lists, please log in to your user account for this.
  • Media type: E-Article
  • Title: Senescence marker protein 30 is up‐regulated in kainate‐induced hippocampal damage through ERK‐mediated astrocytosis
  • Contributor: Son, Tae Gen; Park, Hee Ra; Kim, So Jung; Kim, Keunho; Kim, Min‐Sun; Ishigami, Akihito; Handa, Setsuko; Maruyama, Naoki; Chung, Hae Young; Lee, Jaewon
  • Published: Wiley, 2009
  • Published in: Journal of Neuroscience Research, 87 (2009) 13, Seite 2890-2897
  • Language: English
  • DOI: 10.1002/jnr.22122
  • ISSN: 0360-4012; 1097-4547
  • Origination:
  • Footnote:
  • Description: AbstractSenescence 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.