PMID:10773432

Citation	Hayashi, T, Sakai, K, Sasaki, C, Zhang, WR, Warita, H and Abe, K (2000) c-Jun N-terminal kinase (JNK) and JNK interacting protein response in rat brain after transient middle cerebral artery occlusion. Neurosci. Lett. 284:195-9
Abstract	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 JNK-1 activation might become an innovative means of therapy for stroke treatment in the future.
Links	PubMed
Keywords	Adaptor Proteins, Signal Transducing; Animals; Apoptosis; Carrier Proteins/immunology; Carrier Proteins/metabolism; Cell Nucleus/metabolism; Cerebral Arteries/physiopathology; Cerebral Cortex/blood supply; Cerebral Cortex/metabolism; Cerebral Cortex/pathology; Cytoplasm/metabolism; Enzyme Induction; Immunohistochemistry; Ischemic Attack, Transient/metabolism; Ischemic Attack, Transient/physiopathology; Male; Mitogen-Activated Protein Kinase 8; Mitogen-Activated Protein Kinases/immunology; Mitogen-Activated Protein Kinases/metabolism; Neurons/metabolism; Neurons/pathology; Phosphorylation; Rats; Rats, Wistar; Reperfusion; Time Factors
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Annotations

Gene product	Qualifier	GO Term	Evidence Code	with/from	Aspect	Extension	Notes	Status
RAT:MK08	part_of	GO:0005634: nucleus	ECO:0000314: direct assay evidence used in manual assertion		C		Seeded From UniProt	complete
RAT:MK08	part_of	GO:0005737: cytoplasm	ECO:0000314: direct assay evidence used in manual assertion		C		Seeded From UniProt	complete

References

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