| Project/Area Number |
23790259
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General physiology
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| Research Institution | Osaka Medical College |
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Principal Investigator |
SHIRAIWA Yuka 大阪医科大学, 医学部, 助教 (20596605)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | ClC-5 / V-ATPase / 尿管結石 / Ca輸送障害 / vATPase / NPPB / エンドソーム / CLC-5 / 酸性小胞 |
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| Research Abstract |
It has been reported that dysfunction of ClC-5, Cl- channel, produced the kidney stone. We recently demonstrated that ClC-5 existed in both the proximal and distal tubule cells in the bullfrog, producing the calcium oxalic calculus in the kidney. Therefore, in this experiment, we purposed to clarify the relationship between the changes in Cl- transport and those in H+ or Ca2+ transport in the bullfrog tubule cells. The peritubular perfusion with the inhibitor of Cl- transport, or with low Cl- solution always produced the change in pH in both cytosolic and tubular fluid (pHTF) in proximal tubule or the pHTF in the distal tubule. When the pHTF increases, Ca2+ concentration in tubular fluids ([Ca]TF) always decreases in both proximal and distal tubules, indicating that [Ca]TF is regulated by pHTF against the sedimentation of calcium salt (calculus) in the urine. Thus, Dent's disease caused by dysfunction of ClC-5 might be induced by the change in H+ transport across the tubule cells.
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