| Project/Area Number |
18K15948
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 53030:Respiratory medicine-related
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| Research Institution | Nagoya University |
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Principal Investigator |
Koji Sakamoto 名古屋大学, 医学部附属病院, 病院講師 (00635633)
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| Project Period (FY) |
2018-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2020: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 肺線維症 / エピゲノム / RNA / 細胞老化 / 老化 / lncRNA / ミトコンドリアDNA / ＲＮＡ / リプログラミング / ノンコーディングRNA / エピジェネティクス / 非コードRNA |
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| Outline of Final Research Achievements |
While the importance of cellular senescence in the pathogenesis of idiopathic pulmonary fibrosis, an age-related intractable disease, has attracted much attention, the involvement of long non-coding RNAs (lncRNAs), a new epigenomic factor responsible for cellular fate determination including cellular senescence, remains unclear. We identified a number of lncRNAs that are specifically altered in idiopathic pulmonary fibrosis based on a large-scale comprehensive RNA expression analysis of human lung tissue. We subsequently extracted several lncRNAs that are also involved in cellular senescence. Among them, we focused on FENDRR, a lncRNA specifically expressed in mesenchymal cells, functions to regulate the cellular senescence phenotype of fibroblasts induced by stimuli such as TGF-β and oxidative stress, which is assumed to be mediated partly by the regulation of NADPH oxidase.
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| Academic Significance and Societal Importance of the Research Achievements |
肺線維症の肺組織で発現変化する新規エピゲノム因子・長鎖ノンコーディングRNAが肺細胞において病態形成に関係した病的な細胞変化、特に細胞老化の表現型を制御していることが示唆された。本研究の更なる発展により難治の肺疾患において長鎖ノンコーディングRNAを用いた同疾患の新しい治療標的の開発やバイオマーカーの創出が期待される。
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