Elucidation of epithelial mesenchymal transition and regeneration of lens in posterior capsule opacity after cataract surgery.
| Project/Area Number |
26462672
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
KUBO Eri 金沢医科大学, 医学部, 教授 (10262619)
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| Research Collaborator |
YOSHINO Ayaka
OCHIAI Kana
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 後発白内障 / トロポミオシン / 上皮間葉系移行 / 創傷治癒 / 水晶体上皮細胞 / 後嚢混濁 / FGF |
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| Outline of Final Research Achievements |
In this study, we revealed that Tpm1/2 was related to progression of rat PCO after cataract surgery and other processes of EMT such as wound healing. We showed that stress fiber formation in MLEC induced by EMT could be reversed by FGF2 and Tpm1/2 siRNA transfection. Our results revealed involvement of FGF2-MAPK pathway in FGF2-mediated inhibition of Tpm expression. Furthermore, we investigated the role of Tpm2 in PCO, EMT and lens opacity by generating Tpm2 hetero-knock-out mice. Since Tpm2 is involved in the progression of EMT in LEC wound healing its inhibition may suppress PCO.
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Report
(4 results)
Research Products
(15 results)
