Project/Area Number |
25461253
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Kidney internal medicine
|
Research Institution | Jichi Medical University |
Principal Investigator |
MUTO SHIGEAKI 自治医科大学, 医学部, 教授 (40190855)
|
Co-Investigator(Renkei-kenkyūsha) |
FURUSE MIKIO 自然科学研究機構生理学研究所, 脳形態解析研究部門, 教授 (90281089)
|
Project Period (FY) |
2013-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | claudin / タイトジャンクション / 細胞間短絡路 / 近位尿細管 / 集合管 / 腎臓血管内皮細胞 / claudin-2 / 腎近位尿細管 / ネフロン内不均一性 / claudin-15 / 腎血管内皮細胞 / claudin-8 / 腎集合管 / 傍細胞経路 / Na/Cl輸送 |
Outline of Final Research Achievements |
In mice lacking claudin-2, which is expressed mainly at the proximal tubule tight junction, a reduction in proximal tubule paracellular Na reabsorption may completely compensate by increasing Na reabsorption from the furosemide-, thiazide-, and amiloride-sensitive distal nephron segments. Mice lacking claudin-8, which is expressed at the collecting duct tight junction, exhibited elevated fractional Ca excretion without reduced serum Ca concentrations. Mice lacking claudin-15, which is expressed only at the kidney vascular endothelial cell tight junction, showed hypercalcemia with relatively reduced fractional Ca excretion and hypomagnesemia due to elevated fractional Mg excretion. Future studies will be required to clarify the mechanisms responsible for the observed urine electrolyte disorders in mice lacking claudin-15.
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