Roles of Exosomal miRNA release from lung fibroblasts in the pathogenesis of COPD
| Project/Area Number |
15K19413
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Chiba University |
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Principal Investigator |
Ikari Jun 千葉大学, 大学院医学研究院, 助教 (50734604)
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| Research Collaborator |
Tada Yuji 千葉大学, 大学院医学研究院, 講師 (50344990)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | エクソソーム / マイクロRNA / 肺線維芽細胞 / COPD / 肺繊維芽細胞 |
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| 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.
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Report
(3 results)
Research Products
(2 results)
