| Project/Area Number |
15K18987
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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 pharmacology
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| Research Institution | Osaka University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 慢性腎臓病 / 長鎖ncRNA / 長鎖ノンコーディングRNA / 炎症 |
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| Outline of Final Research Achievements |
Chronic kidney disease (CKD) is a leading cause of kidney failure and cardiovascular diseases. Although there is an unmet medical need for CKD treatments, the mechanisms of physiological and pathological changes of kidney remain to be elucidated. Recently, attention has been drawn to noncoding RNA (ncRNA) as therapeutic targets and biomarkers of diseases. In the present study, we examined the role of MALAT1, long ncRNA, in kidney diseases. The expression of MALAT1 was increased in a mouse model of kidney disease. The kidney injury was suppressed in P2X7R knockout mouse, accompanied by reduced expression of MALAT1. LL37, a ligand of P2X7R, increased MALAT1 expression and induced cell death in cultured podocyte. Our study suggests the possibility that MALAT1, as a downstream signal of LL37/P2X7R, may contribute to cell death in kidney diseases.
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