Roles of Exosomal miRNA release from lung fibroblasts in the pathogenesis of COPD

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K19413
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Respiratory organ internal medicine
• Research Institution: Chiba University
• Principal Investigator: Ikari Jun 千葉大学, 大学院医学研究院, 助教 (50734604)
• Research Collaborator: Tada Yuji 千葉大学, 大学院医学研究院, 講師 (50344990)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: エクソソーム / マイクロRNA / 肺線維芽細胞 / COPD

Outline of Final Research Achievements

In COPD, miR-146a is decreased in lung fibroblasts, leading to reduced repair function. Whether lung fibroblasts release exosomes contain miR-146a and whether this can be modulated by inflammatory cytokines is unclear. Human fetal lung fibroblasts (HFL-1) or primary adult control and COPD lung fibroblasts were cultured with and without IL-1β and TNF-α in vitro. HFL-1 cells secreted exosomes into cultured media both in the presence and absence of IL-1β and TNF-α. Cytokines stimulation significantly increased extracellular miR-146a secretion in a time and concentration dependent manner. Cytokines stimulated both exosomes secretion and intracellular miR-146a expression, leading to the augmented miR-146a release. COPD lung fibroblasts secreted less miR-146a into Exosomes than control lung fibroblasts. The current study demonstrates that lung fibroblasts release extracellular miR-146a, that this is modulated by cytokines and that COPD fibroblasts release less miR-146a.

Free Research Field

COPD