title: Effects of kainate-mediated excitotoxicity on the expression of rat counterparts of A170 and MSP23 stress proteins in the brain.
abstract: Stress proteins play important roles in the protective mechanisms under critical conditions for cell survival. We report here the expression of A170 and MSP23, oxidative stress-inducible proteins, under kainate-mediated excitotoxicity in the rat brain. A170 mRNA was significantly induced in the brain 5-8 h after i.p. kainate administration. MSP23 mRNA was observed at quite a low level in the rat brain, and the induction of MSP23 mRNA was not observed during the period 24 h after kainate administration. Immunoblot analysis demonstrated that the maximal expression level of A170 protein occurred 8 h after treatment in each part of the brain. MSP23 protein was constitutively expressed in the brain and the level of this protein was significantly decreased during the period 24 h after kainate administration. In situ hybridization and immunohistochemical studies showed that A170 was expressed predominantly in neurons, especially in pyramidal neurons of the cerebrum and cerebellar Purkinje cells, while MSP23 was expressed in oligodendrocytes. The induction of A170 was observed in the regions which are affected by excitotoxicity and this induction was observed in the earlier phase than cell death. Also, the region which shows high vulnerability to excitotoxicity such as pyramidal cell layer in the hippocampus, showed lower A170 expression than that which shows resistance to excitotoxicity, such as the dentate gyrus in the hippocampus. These results suggest that A170 may play a protective role in the brain under kainate-mediated excitotoxicity.
authors.affiliation: Department of Biochemistry, Faculty of Medicine, Tottori University, Yonago, Japan. kazuhiro@grapemed.tottori-u.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Nakaso
authors.forename: M
authors.initials: M
authors.lastname: Kitayama
authors.forename: T
authors.initials: T
authors.lastname: Ishii
authors.forename: S
authors.initials: S
authors.lastname: Bannai
authors.forename: T
authors.initials: T
authors.lastname: Yanagawa
authors.forename: K
authors.initials: K
authors.lastname: Kimura
authors.forename: K
authors.initials: K
authors.lastname: Nakashima
authors.forename: E
authors.initials: E
authors.lastname: Ohama
authors.forename: K
authors.initials: K
authors.lastname: Yamada
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D006360:Heat-Shock Proteins / Q000096:biosynthesis; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007608:Kainic Acid / Q000494:pharmacology*; D008297:Male; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D018384:Oxidative Stress / Q000502:physiology*; D010544:Peroxidases; D054464:Peroxiredoxins; D051381:Rats; D017208:Rats, Wistar; D000071456:Sequestosome-1 Protein
chemical_list: D006360:Heat-Shock Proteins; D009419:Nerve Tissue Proteins; D000071456:Sequestosome-1 Protein; C491079:Sqstm1 protein, rat; D010544:Peroxidases; C489898:Prdx1 protein, rat; D054464:Peroxiredoxins; C489899:Prdx1 protein, mouse; D007608:Kainic Acid