Immunoreactive Akt, PI3-K and ERK protein kinase expression in ischemic rat brain

被引:88
作者
Kitagawa, H
Warita, H
Sasaki, C
Zhang, WR
Sakai, K
Shiro, Y
Mitsumoto, Y
Mori, T
Abe, K
机构
[1] Okayama Univ, Sch Med, Dept Neurol, Okayama 7008558, Japan
[2] Otsuka Pharmaceut Co Ltd, Tokushima New Drug Res Inst, Tokushima 7710192, Japan
关键词
Akt-1; PI3-K; ERK-1; MCAO; ischemia; rats; immunoreactivity;
D O I
10.1016/S0304-3940(99)00676-X
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
In order to clarify the role of protein kinases in ischemic brain injury, the spatiotemporal expression of immunoreactive serine-threonine kinase AM, phosphatidylinositol 3-kinase (P13-K) and extracellular signal-regulated kinase (ERK) were examined at 3, 8, or 24 h after permanent middle cerebral artery occlusion (MCAO) in rats. Weak staining for these protein kinases was found in both cortical and caudate neurons in sham controls. The staining for Akt-1 and P13-K was increased at 3-8 h in the ischemic penumbral region and declined at 24 h. A slight induction of these kinases was observed in the ischemic core region. Robust expression of ERK was noted at 3-8 h in most neurons in the area of ischemia. At 24 h, ERK continued to be expressed in the ischemic penumbra, but decreased in the ischemic core, These findings suggest that the signaling for Akt and P13-K are different from the ERK dependent signal transduction during ischemic brain injury. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:45 / 48
页数:4
相关论文
共 21 条
  • [1] Expression of the glial cell line-derived neurotrophic factor gene in rat brain after transient MCA occlusion
    Abe, K
    Hayashi, T
    [J]. BRAIN RESEARCH, 1997, 776 (1-2) : 230 - 234
  • [2] Anderson CNG, 1999, J NEUROSCI, V19, P664
  • [3] ERKS - A FAMILY OF PROTEIN-SERINE THREONINE KINASES THAT ARE ACTIVATED AND TYROSINE PHOSPHORYLATED IN RESPONSE TO INSULIN AND NGF
    BOULTON, TG
    NYE, SH
    ROBBINS, DJ
    IP, NY
    RADZIEJEWSKA, E
    MORGENBESSER, SD
    DEPINHO, RA
    PANAYOTATOS, N
    COBB, MH
    YANCOPOULOS, GD
    [J]. CELL, 1991, 65 (04) : 663 - 675
  • [4] Apoptosis and necrosis after reversible focal ischemia: An in situ DNA fragmentation analysis
    CharriautMarlangue, C
    Margaill, I
    Represa, A
    Popovici, T
    Plotkine, M
    BenAri, Y
    [J]. JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1996, 16 (02) : 186 - 194
  • [5] Crowder RJ, 1998, J NEUROSCI, V18, P2933
  • [6] Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery
    Datta, SR
    Dudek, H
    Tao, X
    Masters, S
    Fu, HA
    Gotoh, Y
    Greenberg, ME
    [J]. CELL, 1997, 91 (02) : 231 - 241
  • [7] Dudek H, 1997, AKT SCI, V275, P661
  • [8] Translocation and down-regulation of protein kinase C-α, -β, and -γ isoforms during ischemia-reperfusion in rat brain
    Harada, K
    Maekawa, T
    Abu Shama, KM
    Yamashima, T
    Yoshida, K
    [J]. JOURNAL OF NEUROCHEMISTRY, 1999, 72 (06) : 2556 - 2564
  • [9] Expression of cyclin-dependent kinase 5 and its activator p35 in rat brain after middle cerebral artery occlusion
    Hayashi, T
    Warita, H
    Abe, K
    Itoyama, Y
    [J]. NEUROSCIENCE LETTERS, 1999, 265 (01) : 37 - 40
  • [10] Inductions of hepatocyte growth factor and its activator in rat brain with permanent middle cerebral artery occlusion
    Hayashi, T
    Abe, K
    Sakurai, M
    Itoyama, Y
    [J]. BRAIN RESEARCH, 1998, 799 (02) : 311 - 316