| Project/Area Number |
24659264
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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 |
Applied pharmacology
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
NAGAI Takako 金沢医科大学, 大学病院, 医員 (90625443)
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| Co-Investigator(Kenkyū-buntansha) |
KANASAKI Keizo 金沢医科大学, 医学部, 講師 (60589919)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | EndMT / AcSDKP / 糖尿病性腎症 |
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| Outline of Final Research Achievements |
The fibroblasts play a role in kidney fibrosis. Recently, the endothelial-to-mesenchymal transition (EndMT) has emerged as an important source of myofibroblasts or activated fibroblasts. MicroRNA let-7 exhibits anti EndMT effects and fibroblast growth factor (FGF) receptor has been shown to be an important in microRNA let-7 expression. We found that the endogenous anti fibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) inhibited the EndMT and exhibited anti fibrotic effects; Such anti fibrotic effects of AcSDKP were associated with FGF receptor mediated anti-fibrotic program. Regards with this, endogenous levels of AcSDKP were suppressed in the urine of streptozotocin-induced diabetic CD-1 mice.
These results suggest that AcSDKP is an endogenous anti fibrotic molecule that has the potential to cure diabetic kidney fibrosis via an inhibition of the EndMT associated with the restoration of FGF receptor and microRNA let-7.
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