| Project/Area Number |
26461199
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Juntendo University |
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Principal Investigator |
Sato Tadashi 順天堂大学, 医学部, 准教授 (10596993)
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| Co-Investigator(Kenkyū-buntansha) |
瀬山 邦明 順天堂大学, 医学部, 先任准教授 (10226681)
高橋 史行 順天堂大学, 医学部, 准教授 (70327823)
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| Co-Investigator(Renkei-kenkyūsha) |
ISHIGAMI Akihito 東京都健康長寿医療センター研究所, 老化制御研究チーム, 研究部長 (50270658)
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| Research Collaborator |
RENNARD Stephen I. ネブラスカ大学, 医療センター, 教授
SUZUKI Yohei 順天堂大学, 医学部, 助教
MITSUI Aki 順天堂大学, 医学部, 実験助手
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | microRNA / 慢性閉塞性肺疾患(COPD) / miR-146a / 喫煙 / 炎症 / COX-2 / IL-8 / エクソソーム / 気管支洗浄液 / 気道上皮細胞 / タバコ煙抽出液 / COPD増悪 / NF-kB / SMP30ノックアウトマウス |
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| Outline of Final Research Achievements |
Cigarette smoking is the most important cause of COPD, but the mechanisms of pathogenesis are incompletely defined. We have reported that a specific microRNA, miR-146a, plays a pathogenetic role in the abnormal inflammatory response in COPD. In the current study, we investigated the role of miR-146a in acute phase of inflammatory response towards cigarette smoking. Interleukin-8 was significantly increased in BEAS-2B cells, normal human bronchial epithelial cells, following 6 days of cigarette smoke extract (CSE) and 2 days of lipopolysaccharide (LPS) compared with non-CSE treatment cells (70.2→118.1 pg/mL, P<0.01). Additionally, LPS-induced miR-146a expression was also increased significantly by pretreatment of CSE (relative expression: 44.0→70.1, P<0.01). Together, LPS-induced inflammatory response was clearly enhanced by CSE pretreatment in human bronchial epithelial cells. Moreover, miR-146a may associate with the acute inflammatory response during the exacerbation of COPD.
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