| Project/Area Number |
17K16103
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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 |
Kidney internal medicine
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| Research Institution | St. Marianna University School of Medicine |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2019: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | 急性腎障害 / ポリコームグループタンパク質 / SCMH1 / 虚血耐性 / 腎保護作用 / 腎臓内科 / 腎臓 / 内科 / 細胞・組織 |
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| Outline of Final Research Achievements |
Frequency of onset of iatrogenic acute kidney injury (AKI) is increasing under development of medical technology in as aging society. However, such a AKI has few curative treatments. The aim of this study was to reveal a role of polycomb group protein (Bmi1 and SCMH1) under hypoxia which is a main cause of iatrogenic AKI. Because proximal tubular cells are principle target for the AKI, human proximal tubular cells (HK2 cells) were used. Down-regulation of SCMH1 by siRNA for SCMH1 induced increase in cytotoxicity and decrease in cell survival rate. However, such a result was not found by down-regulation of Bmi1 by siRNA for Bmi1.The SCMH1 expressed in the proximal tubule may have a protective effect against hypoxia.
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| Academic Significance and Societal Importance of the Research Achievements |
高齢者の増加、医療技術の進歩により、医原性の急性腎障害(AKI)の発症頻度が、世界的に増加しているものの、その有効な治療法がないため、ポリコームグループタンパク質（PRC1構成蛋白 Bmi1およびSCMH1)に着目し、その細胞保護作用の有無を検討した。その結果、SCMH1が、腎保護的に作用する事が明らかになった。SCMH1の発現増強は、AKI治療に有効である可能性があり、さらなる検討を行う。
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