| Project/Area Number |
25660241
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Veterinary medical science
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| Research Institution | University of Miyazaki |
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Principal Investigator |
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| Research Collaborator |
MATSUZAKI Toshiyuki
SONODA Hiroko
TAKAHASHI Saki
HIGASHIJIMA Yoshiki
SHIGEMURA Kanako
KAITO Ayaha
KATO Ayaka
KINOUCHI Minami
HOSHINO Yuya
KOGA Moeko
MIKODA Nobuyuki
ASVAPROMTADA Siree
OSHIKAWA Sayaka
HONBU Anna
ABDEEN Ahmed
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | エクソソーム / 小胞体ストレス / 腎疾患 / アクアポリン |
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| Outline of Final Research Achievements |
Several previous reports have indicated that endoplasmic reticulum (ER) stress is related to renal diseases. In order to find a new biomarker for ER stress in the kidney, we pharmacologically examined the urinary exosomal proteins in rats and cultured cells. Among proteins tested in this study, only the urinary exosomal releasel of AQP1 was markedly decreased by the treatment with tunicamycin (an ER stress inducer). Tunicamycin also decreased the level of AQP1 mRNA in the kidney. When either tunicamycin or thapsigargin (another ER stress inducer) was added to cultured renal proximal tubule cells, down-regulation of AQP1 mRNA was observed. These findings indicates that ER stress decreases the urinary exosomal excretion of AQP1 protein and the underlying mechanism is mediated by lowering the level of renal AQP1 mRNA, suggesting that urinary exosomal AQP1 is a possible biomarker for detection of ER stress in the kidney.
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