Mechanism of pulmonary fibrosis induced by deranged fatty acid composition

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K15456
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Respiratory organ internal medicine
• Research Institution: Gunma University
• Principal Investigator: Kurabayashi Masahiko 群馬大学, 大学院医学系研究科, 教授 (00215047)
• Co-Investigator(Kenkyū-buntansha): 前野 敏孝 群馬大学, 医学部附属病院, 講師 (00436297)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: 脂肪酸 / サーファクタント / 線維化 / 肺気腫 / 飽和脂肪酸

Outline of Final Research Achievements

In the present study, we demonsrated that the lack of Elovl6 has a causative role in lung pathology. Apoptosis and ROS production were increased in Elovl6－/－ lung. Alveolar type II epithelial cells isolated from Elovl6－/－ mice and LA-4 cells produced increased levels of ROS. Elovl6 deficiency increased PA and decreased OA and PUFA content in alveolar type II epithelial cells both in vivo and in vitro. Expressions of the genes for FADS1, FADS2, FATPs and FAT/CD36 were significantly reduced in Elovl6－/－ mice, suggesting that cellular uptake of long-chain FAs, including PUFA, was impaired in Elovl6－/－ mice.

Free Research Field

循環器内科学