| Project/Area Number |
16H06962
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Periodontology
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| Research Institution | Osaka University |
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Principal Investigator |
Ikegami Kuniko 大阪大学, 歯学部附属病院, 医員 (80779116)
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| Research Collaborator |
YAMASHITA MOTOZO 大阪大学, 歯学部附属病院, 講師 (90524984)
MURAKAMI SHINYA 大阪大学, 歯学研究科, 教授 (70239490)
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| Project Period (FY) |
2016-08-26 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 歯周病 / 老化 / 歯学 |
|---|
| Outline of Final Research Achievements |
Periodontitis is characterized as an age-dependent chronic disease with tissue destruction caused by dental plaque. Accumulation of environmental stress, such as bactericidal infection, ROS and traumatic occlusal force is thought to induce senescence in periodontal tissue at cellular level. We previously reported that senescent human periodontal ligament cells (HPDL) secrete various inflammatory cytokines, referred to as the senescence-associated secretory phenotype (SASP). Moreover, senescent HPDL showed the diminished stem cell property. A comprehensive analysis of microRNA identified miR-34a which is preferentially expressed in senescent HPDL as a regulator of cellular senescence. While miR-34a expression was elevated, SIRT1 expression was decreased in senescent HPDL. Exogenous miR-34a treatment induced IL-6 production in HPDL by targeting SIRT1. miR-34a-SIRT1 pathway may participate in stem-cell aging in senescent HPDL.
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