| Project/Area Number |
21790815
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Kidney internal medicine
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KIDO Shinsuke 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 特任助教 (30437652)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 老化 / 腎不全 / 骨不全 / 血管石灰化 / 骨粗鬆症 |
|---|
| Research Abstract |
Oxidative stress reduces osteoblast number and suppresses bon formation, leading to the age-related loss of bone. We have demonstrated that anti-adipogenic cytokine, IL-11, is expressed in osteoblasts in an AP-1-dependent manner, and that DNA binding activity of JunD was reduced without change in its protein level in aged mice. Therefore, there is a possibility that reduced JunD activity may be caused by post-translational modification of JunD by an age-related increase in oxidative stress. In the present study, we showed that MBF1 protein was expressed in all tissues examined, whereas the amount of MBF1 decreased in many tissues including bone of aged mice. Besides, DNA precipitation assay demonstrated that MBF1 forms complex with JunD on an AP-1 site of IL-11 promoter via binding to a basic region of JunD. MBF1 binding to JunD also enhanced AP-1-dependnt IL-11 gene transcription even in the presence of hydrogen peroxide. It is suggested that reduced MBF1 protein expression in osteoblasts may play a role in age-related impairment of osteoblast differentiation by suppressing IL-11 transcription via a reduction in JunD activity, and that MBF1 can be a new target against age-related loss of bone.
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