| Project/Area Number |
26861461
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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 | Kyoto Prefectural University of Medicine |
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Principal Investigator |
Nakatsukasa Mina 京都府立医科大学, 医学(系)研究科(研究院), 客員講師 (70614022)
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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 |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 膠様滴状角膜ジストロフィ / TACSTD2 / CLDN1 / CLDN7 / タイトジャンクション / PKC-α / 二次性角膜アミロイドーシス / 二次性角膜アミロイド―シス |
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| Outline of Final Research Achievements |
In the cornea of secondary corneal amyloidosis which indicates a clinical image similar to gelatinous drop like dystrophy (GDLD), TACSTD2, CLDN1 and CLDN7 proteins were found, which suggests the possibility that a mechanism of amyloid deposition to cornea of secondary corneal amyloidosis is different from GDLD.
The expression level of PKC-α in immortalized human GDLD corneal epithelial cells (iHGCEpi) and immortalized human GDLD conjunctival epithelial cells were highly expressed compared to corneal and conjunctival epithelial cells derivered from a normal patient. And the expression level of CLDN1 and CLDN7 proteins in iHGCEpi was recovered after the transduction of TACSTD2 gene, while PKC-α was significantly decreased by transducing of TACSTD2 gene.
Further, the expression level of PKC-α was decreased, and CLDN1 and CLDN7 were recovered in iHGCEpi by the treatment of PKC-α inhibitor. In summary, relationship of PKC-α was indicated in the pathological process of GDLD.
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