c-Jun N-terminal kinase (JNK) and JNK interacting protein response in rat brain after transient middle cerebral artery occlusion

被引:69
作者
Hayashi, T [1 ]
Sakai, K [1 ]
Sasaki, C [1 ]
Zhang, WR [1 ]
Warita, H [1 ]
Abe, K [1 ]
机构
[1] Okayama Univ, Sch Med, Dept Neurol, Okayama 7008558, Japan
关键词
c-Jun N-terminal kinase; c-Jun N-terminal kinase interacting protein; immunohistochemistry; ischemia; rat;
D O I
10.1016/S0304-3940(00)01024-7
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
c-Jun response is involved in the development of ischemic brain injury, which is activated by c-Jun N-terminal kinase-1 (JNK-1). The activity of JNK-1 is strictly regulated, and only the phosphorylated form of JNK (phospho-JNK) which is translocated to the nucleus has an ability to activate c-Jun response. There is a protein which inhibits JNK-1 activation, and known as JNK interacting protein-1 (JIP-1). In this study, we investigated change in JNK-1, phospho-JNK, and JIP-1 immunoreactivity in rat brain after transient middle cerebral artery (MCA) occlusion. Immunoreactive JNK-1 was scant in the sham-control brain, but it was induced at 1 h after reperfusion, which was slightly increased at 3 h of reperfusion. By contrast, phospho-JNK remained negative till 3 h. At 8 h, JNK-1 and phospho-JNK became distinctly positive, and nuclei as well as cytoplasm were stained. Thereafter, immunoreactivity for JNK-1 and phospho-JNK became furthermore dense, and most neurons revealed positively stained nuclei. Immunoreactivity for JIP-1 remained negative till 8 h of reperfusion, but at 24 and 72 h, cytoplasm of cortical neurons at the MCA boundary area was positively stained. This JIP-1 induction got behind the JNK-1 activation, and therefore, may be a vain effort for neurons to survive. inhibition of JNK1 activation might become an innovative means of therapy for stroke treatment in the future. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:195 / 199
页数:5
相关论文
共 18 条
[1]   Expression of interleukin-1 beta converting enzyme gene family and bcl-2 gene family in the rat brain following permanent occlusion of the middle cerebral artery [J].
Asahi, M ;
Hoshimaru, M ;
Uemura, Y ;
Tokime, T ;
Kojima, M ;
Ohtsuka, T ;
Matsuura, N ;
Aoki, T ;
Shibahara, K ;
Kikuchi, H .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1997, 17 (01) :11-18
[2]   Differential regulation of apoptosis-related genes in resistant and vulnerable subfields of the rat epileptic hippocampus [J].
Becker, AJ ;
Gillardon, F ;
Blümcke, I ;
Langendörfer, D ;
Beck, H ;
Wiestler, OD .
MOLECULAR BRAIN RESEARCH, 1999, 67 (01) :172-176
[3]  
BRECHT S, 1998, PHARM CEREBRAL ISCHE, P151
[4]   Apoptosis and necrosis after reversible focal ischemia: An in situ DNA fragmentation analysis [J].
CharriautMarlangue, C ;
Margaill, I ;
Represa, A ;
Popovici, T ;
Plotkine, M ;
BenAri, Y .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1996, 16 (02) :186-194
[5]  
Chen SC, 1996, ADV NEUROL, V71, P433
[6]   A cytoplasmic inhibitor of the JNK signal transduction pathway [J].
Dickens, M ;
Rogers, JS ;
Cavanagh, J ;
Raitano, A ;
Xia, ZG ;
Halpern, JR ;
Greenberg, ME ;
Sawyers, CL ;
Davis, RJ .
SCIENCE, 1997, 277 (5326) :693-696
[7]  
Eilers A, 1998, J NEUROSCI, V18, P1713
[8]   ALTERED GENE-EXPRESSION IN NEURONS DURING PROGRAMMED CELL-DEATH - IDENTIFICATION OF C-JUN AS NECESSARY FOR NEURONAL APOPTOSIS [J].
ESTUS, S ;
ZAKS, WJ ;
FREEMAN, RS ;
GRUDA, M ;
BRAVO, R ;
JOHNSON, EM .
JOURNAL OF CELL BIOLOGY, 1994, 127 (06) :1717-1727
[9]   Expression of cell death-associated phospho-c-Jun and p53-activated gene 608 in hippocampal CA1 neurons following global ischemia [J].
Gillardon, F ;
Spranger, M ;
Tiesler, C ;
Hossmann, KA .
MOLECULAR BRAIN RESEARCH, 1999, 73 (1-2) :138-143
[10]   TRANSCRIPTION FACTOR ATF2 REGULATION BY THE JNK SIGNAL-TRANSDUCTION PATHWAY [J].
GUPTA, S ;
CAMPBELL, D ;
DERIJARD, B ;
DAVIS, RJ .
SCIENCE, 1995, 267 (5196) :389-393