Study on interaction of intracellular signal in renal tubularinterstitial fibrosis
Project/Area Number |
22590896
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Kidney internal medicine
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Research Institution | Wakayama Medical University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
MURAGAKI Yasuteru 和歌山県立医科大学, 医学部, 教授 (40190904)
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Project Period (FY) |
2010 – 2012
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Project Status |
Completed (Fiscal Year 2012)
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Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | 腎臓 / 間質線維化 / Trps1 / EMT / MET / 線維化 / TGF-beta / BMP7 / 上皮間葉転換 / 腎 / TGF-βシグナル / Smad3 / Arkadia / Smad7 / TGF-Bシグナル / Trpsl |
Research Abstract |
To study the interaction between Bmp7 and TGF-β intracellular signaling in renal tubular interstitial fibrosis, we used a mouse fibrosis model by unilateral ureteral obstruction (UUO). We compared the degree of renal tubular intestinal fibrosis caused by UUO using wild -type (WT) and Trps1 heterozygous KO (HT) mice. HT mice had more severe fibrosis than WT mice. From this experiment, we concluded that Trps1 functions downstream of Bmp7 and suppresses fibrosis by inhibiting Arkadia expression, suppressing TGF-β signaling.
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Report
(4 results)
Research Products
(41 results)
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[Presentation] Masahiko Kuroda , Yasuteru Muragaki.Wapl regulates HP1 expression and levels of various histone H3 tail modifications2012
Author(s)
Kosuke Oikawa, Masakatsu Takanashi, Mayako Niwa, Yujing Sun, Ting Gui, Aiko Shimokado, Shunji Itoh , Takashi Ozaki, Masahiko Kuroda , Yasuteru Muragaki
Organizer
日本分子生物学会年会
Place of Presentation
福岡市
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