2003 Fiscal Year Final Research Report Summary
Mechanism of water transport; Elucidation of brain edema and development of treatment.
| Project/Area Number |
12557232
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
応用薬理学・医療系薬学
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| Research Institution | SAPPORO MEDICAL UNIVERSITY |
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Principal Investigator |
HORIO Yoshiyuki Sapporo Medical University, MD, PhD., Professor, 医学部, 教授 (30181530)
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| Co-Investigator(Kenkyū-buntansha) |
SAKAMOTO Jun Sapporo Medical University, MD, PhD., Assistant Professor, 医学部, 助手 (40336392)
TAKEMURA Haruo Sapporo Medical University, PhD., Lecturer, 医学部, 講師 (20106462)
HATTA Shinnichi Sapporo Medical University, PhD., Associate Professor, 医学部, 助教授 (60094223)
INUZUKA Eiji Hamamatsu Photonics K.K., PhD., Director, 医学部, 部長
HISAKARA Shin Sapporo Medical University, MD, PhD., Assistant Professor, 医学部, 助手 (80336403)
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| Project Period (FY) |
2000 – 2003
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| Keywords | water channel / AQP4 / laminine / brain / glia / herbimycin / K^+ channel / ATP sensitive K^+ channel |
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| Research Abstract |
We have studied the distribution of AQP4 water channel in Muller cells, dominant glial cells of the retina, using primary culture of Muller cells. When the cells were cultured on poly lysine-coated glass, AQP4 located in the cytoplasm. We could not find any expression of AQP4 on the membranes. However, when Muller cells were planted on laminine-coated glass, AQP4 was found on the membranes. Expression of AQP4 on the membranes of Muller cells disappeared in the presence of Herbimycin, a thyrosine kinase inhibitor. Extracellular matrix regulates water channel expression on the membranes through the function of a tyrosine kinase. Thus, brain damage causing functional disorder of extracellular matrix may affect surface expression of AQP4 and induce unbalance of water. transport.
Water transport is accompanied with ion transport. Previous experiment showed K^+ channels are important for water transport. We have studied ATP sensitive K^+ channels(KATP channels), because KATP channels open when cells have damage. We found that KATP channels expressed in neurons. Expression of subfamily of KATP channels was different in a neuron. We found that SUR1 subunit existed in the cell body, while SUR2 subunit located in terminals of neuritis. The difference of expression may indicate functional difference of KATP channel subunit.
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