2018 Fiscal Year Final Research Report
Effect of low concentration fluoride in senescence of mesenchymal stem cells
Project/Area Number |
16K11898
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Social dentistry
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Research Institution | Nihon University |
Principal Investigator |
NASU Ikuo 日本大学, 松戸歯学部, 客員教授 (80112952)
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Co-Investigator(Kenkyū-buntansha) |
有川 量崇 日本大学, 松戸歯学部, 教授 (50318325)
Bhawal Ujjal 日本大学, 松戸歯学部, 助教 (50433339)
田口 千恵子 日本大学, 松戸歯学部, 助手(専任扱) (80434091)
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Project Period (FY) |
2016-04-01 – 2019-03-31
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Keywords | 老化 / 間葉系幹細胞 |
Outline of Final Research Achievements |
We evaluated the influence of microRNAs and their target genes on bone tissue to elucidate physiological function of aging in term of bone metabolism and autoimmunity. Total RNA was isolated from femoral tissue using 3-month-old and 15-month-old SAM mice of the aging model. Their gene expression and miRNA expression findings were analyzed using DNA microarrays and miRNA arrays in combination with GeneSpring and Ingenuity Pathways Analysis. Gene ontology (GO) analysis revealed that it incorporates critical transcription-related processes and intracellular signaling of genes targeted to miRNA. Further analysis by RT-qPCR indicates that aging regulatory transcription factors are involved in the regulation of miR-223-3p, miR-744-5p, miR-3103-5p, miR-4723-5p and miR-6825-5p. Comprehensive analysis of mRNAs and miRNAs in which numerous combinations were identified suggested that aberrant expression of miRNAs is important in bone aging.
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Free Research Field |
口腔衛生学
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Academic Significance and Societal Importance of the Research Achievements |
今回用いるSAMP6系は、若齢期の最大骨密度が低いために加齢に伴い早期に骨粗鬆症に至りやすい老人性骨粗鬆症モデル動物である。当該研究において老化細胞マスター転写因子が制御している標的遺伝子による老化細胞の制御機構を明らかにするため、SAMP6マウスを用いてゲノムワイドにスクリーニングを展開し老化細胞制御遺伝子を同定、骨組織への影響を明らかにすることで、老化幹細胞の生理的機能の解明のみならず、異常活性および機能不全で誘発される代謝性、自己免疫性骨疾患のメカニズム解明し、再生医療の発展に役立つものと考えられる。
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