Basis for chronobiological approach in treatment of corneal nerve damage
| Project/Area Number |
26861456
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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 |
Ophthalmology
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| Research Institution | Oita University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 体内時計 / 時計遺伝子 / マイトマイシンC / グルココルチコイド / 神経障害 |
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| Outline of Final Research Achievements |
Mitomycin C (MMC), which has been applied in surgery of glaucoma or pterygium to suppress growth of fibroblasts, could induce corneal nerve damage. Circadian rhythm of physiological function is regulated by particular gene cluster called as clock gene, which is component of molecular clock. In this study, we performed in vitro study to clarify the possibility of MMC induced dysfunction of circadian clock and relationship between circadian clock dysfunction and corneal nerve damage. The mouse fibroblast cell line NIH3T3 or primary fibroblasts from Per2::Luc knock in mice were used for experiments. MMC decreased expression of glucocorticoid receptor and modulated circadian oscillation of Per2::Luc bioluminescence. These results suggest that MMC could persistently modulate the circadian clock system in fibroblast of eyes.
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Report
(3 results)
Research Products
(14 results)
