Molecular mechanisms of exacerbation effects on mouse lung fibrosis induced by diesel exhaust particles

2014 Fiscal Year Final Research Report

• Project/Area Number: 24590764
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Hygiene
• Research Institution: Nippon Medical School
• Principal Investigator: LI YINGJI 日本医科大学, 医学部, 講師 (60350039)
• 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)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: EMT / DEP / oxidative stress

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.

Free Research Field

環境医学