| Project/Area Number |
24590764
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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 |
Hygiene
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| Research Institution | Nippon Medical School |
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Principal Investigator |
LI YINGJI 日本医科大学, 医学部, 講師 (60350039)
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| Co-Investigator(Kenkyū-buntansha) |
KAWADA Tomoyuki 日本医科大学, 大学院医学研究科, 教授 (00224791)
AZUMA Arata 日本医科大学, 医学部, 教授 (10184194)
INAGAKI Hirofumi 日本医科大学, 医学部, 講師 (50213111)
HIRATA Yukiyo 日本医科大学, 医学部, 助教 (40322515)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | EMT / DEP / oxidative stress / 酸化ストレス / ディーゼル排気粒子 / 細胞遊走能 / 細胞内シグナル伝達 / ＥＭＴ / 細胞遊走 |
|---|
| Outline of Final Research Achievements |
The accumulation of fibroblasts plays a critical role in the development of pulmonary fibrosis. Epithelial-mesenchymal transition (EMT) process is related with pulmonary fibrosis progression. The current study was designed to explore the role of Diesel exhaust particle (DEP) whether or not induce EMT process in airway epithelial cells by oxidative stress. In the bronchial epithelial cell line, E-cadherin expression was down-regulated and N-cadherin expression was up-regulated by DEP exposure. The EMT cells migration was significantly increased and the antioxidant enzymes mRNA expression was up-regulated by DEP. These changes by DEP exposure were blocked by N-acetylcysteine pretreatment. Our results suggest that DEP may exacerbate the tissue remodeling processes of pulmonary fibrosis by oxidative stress.
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