Ischemia induces metallothionein III expression in neurons of rat brain
Autor: | Hiroaki Miyazaki, Yohji Ueno, Shingo Yanagitani, Yoshitsugu Nakahashi, Shigeru Taketani, Yuji Naitoh, Kenji Kuno, Kyoichi Inoue, Masanori Matsushita |
---|---|
Rok vydání: | 1999 |
Předmět: |
Male
Cerebellum Pathology medicine.medical_specialty Time Factors Recombinant Fusion Proteins Genetic Vectors Ischemia Hippocampus Enzyme-Linked Immunosorbent Assay Nerve Tissue Proteins Biology General Biochemistry Genetics and Molecular Biology Brain ischemia medicine Animals RNA Messenger General Pharmacology Toxicology and Pharmaceutics Cloning Molecular Rats Wistar Neurons Cerebrum Dentate gyrus Antibodies Monoclonal Brain General Medicine medicine.disease Blotting Northern Immunohistochemistry Metallothionein 3 Olfactory bulb Cell biology Rats Up-Regulation medicine.anatomical_structure nervous system Cerebral cortex Ischemic Attack Transient |
Zdroj: | Life sciences. 64(8) |
ISSN: | 0024-3205 |
Popis: | Metallothionein III (MT-III) is a brain-specific member of the metallothionein family and binds zinc in vivo. In order to confirm the precise localization of MT-III in normal rat brain and the change of MT-III expression after transient whole brain ischemia, we raised a high affinity phagemid-antibody specific for rat MT-III. Immunohistochemical analysis revealed that MT-III in normal brain is localized abundantly in neuronal cell bodies in CA1-3 regions of hippocampus, dentate gyrus, cerebral cortex, olfactory bulb and Purkinje cells in cerebellum. This expression pattern of MT-III was similar to that of MT-III mRNA observed by in situ hybridization studies. ELISA and Northern blot analysis revealed that MT-III protein as well as mRNA levels were up-regulated in cerebrum soon after ischemic stress. Immunohistochemical analysis also demonstrated intense staining in neurons in injured brain after ischemia, which distributed in the same regions as in normal brain. These results suggest that MT-III plays an important role in protecting neurons from ischemic insult by reducing neurotoxic zinc levels and inhibits uncontrolled growth of neurites after ischemia. |
Databáze: | OpenAIRE |
Externí odkaz: |