Mechanism of production and release of tissue plasminogen activator in airway epithelial cells
Project/Area Number |
15K10779
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Otorhinolaryngology
|
Research Institution | University of Fukui |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
高林 哲司 福井大学, 学術研究院医学系部門(附属病院部), 講師 (70397272)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
Keywords | 鼻ポリープ / t-PA / レチノイン酸 / 好酸球性副鼻腔炎 / 線溶系 / retinoic acid / 気道上皮細胞 / NHBE / IL-13 |
Outline of Final Research Achievements |
We have evaluated patients with AERD had even lower levels of RA in their nasal polyp tissue compared with CRSwNP. It is tempting to speculate that RA might be necessary for basic production and secretion of t-PA and may regulate fibrin deposition in normal tissue. We have studied the regulation of t-PA production in airway epithelial cells by cytokines and retinoic acid, a topic not researched ever. Retinoic acid, an active metabolite of vitamin A, induced a dose dependent increase of t-PA expression by NHBE cells; most t-PA produced was released into the supernatant. We confirmed the previous finding that IL-13 suppresses t-PA expression and have also shown that RA can restore t-PA expression in IL-13-treated cells. Finally, our results suggest that supplementation of polyposis patients with retinoids might shrink polyps or prevent recurrence of polyps after surgery by inducing t-PA and promoting degradation of fibrin deposited within polyps.
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Report
(4 results)
Research Products
(11 results)