| Co-Investigator(Kenkyū-buntansha) |
SHIMADA Syoichi Nagoya City University Graduate School of Medical Sciences, Professor, 大学院・医学研究科, 教授 (20216063)
AIHARA Noritaka Nagoya City University Graduate School of Medical Sciences, Research Associate, 大学院・医学研究科, 助手 (00264739)
MASE Mitsuhito Nagoya City University Graduate School of Medical Sciences, Assistant Professor, 大学院・医学研究科, 講師 (60238920)
ASAI Kiyofumi Nagoya City. University Graduate School of Medical Sciences, Professor, 大学院・医学研究科, 教授 (70212462)
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| Research Abstract |
To detect changes in channel transporter, we used models of cerebral ischemia, cold-induced edema, subarachnoid hemorrhage (SAH) and intracerebral hemorrhage in rat. The transporters we detected are aquaporin type 1, 4,5 and 8, and myoinositol osmolyte transporter. In the cerebral ischemia, aquaporin type 4 mRNA is expressed in 3 to 7 days after ischemia, and aquaporin type 4 protein is increased in soma and disappearing from vascular foot, indicating turnover of aquaporin 4 is occurring. Similar findings are detected in the cold-induced edema model, indicating that aquaporin type 4 is functioning for resolution of brain edema. On the other hand aquaporins 1,4,5 and 8 is expressed in the cultured astrocyte exposed to hypoxia, indicating multipotential nature of aquaporins. Myoinositol transporter, one of the osmolyte transporters, is expressed in the neurons facing subarachnoid blood of SAH model, indicating osmotic pressure changes in SAH. Myoinositol transporter mRNA is also expressed in the neurons exposed to transient ischemia after SAH, indicating osmolyte changes in cerebral ischemia. We have detected cell death in substantial nigra after striatal hemorrhage in rat. During this process nigral neurons expressed myoinositol mRNA expression, which may relate to cell death. In Summary, channel transporter plays important role in brain injury and its recovery. Treatment trial must be focused in this area.
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