| Project/Area Number |
15K19439
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Respiratory organ internal medicine
|
|---|
| Research Institution | National Center for Child Health and Development |
|---|
Principal Investigator |
Igarashi Arisa 国立研究開発法人国立成育医療研究センター, 免疫アレルギー・感染研究部, (非)研究員 (60572998)
|
|---|
| Research Collaborator |
OKAMURA Kohji
MATSUDA Akio
MATSUMOTO Kenji
|
|---|
| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
|---|
| Keywords | microRNA / 上皮細胞 / 喘息 / miR-29 / sST2 / IL33 / miRNA / アレルギー / 自然免疫 / ぜんそく |
|---|
| Outline of Final Research Achievements |
To identify miRNAs that regulate expression of IL-33, an important cytokine gene for asthma development, expression of miRNAs in human airway epithelial cells was investigated. Consequently, although a novel miRNA directly controlling IL-33 expression could not be identified, miR-29 was found to regulate epithelial expression of both soluble ST2 (sST2), a decoy receptor for IL-33, and IFNAR1, a type 1 interferon receptor. Furthermore, I found that miR-29 is produced extracellularly via exosomes secreted by airway epithelial cells.
These results suggest that miR-29 may be involved in the IL-33-dependent molecular mechanisms of asthma development, triggered by respiratory viral infection, via regulation of sST2 and IFNAR1 expression in the airway epithelial cells.
|
