2013 Fiscal Year Final Research Report
The elucidation of the mechanism suppressing the degradation of claudin proteins by the TACSTD2 protein
| Project/Area Number |
24791868
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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, 医学部附属病院, 専攻医 (70614022)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Keywords | 膠様滴状角膜ジストロフィ / TACSTD2 / タイトジャンクション |
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| Research Abstract |
The TACSTD2 protein identified as a causative gene for Gelatinous Drop-Like Corneal Dystrophy (GDLD) was directly bound to CLDN1 and CLDN7 proteins, and we found that extracellular region of the TACSTD2 protein is essential for its binding to the CLDN7 protein. We also found that AxxxG motif in the transmembrane domain is important for the binding of the TACSTD2 protein to the CLDN7 protein. Although the TJP1 protein expression level was found to be somewhat more reduced in the GDLD cornea than in the normal human cornea, the TJP1 protein was observed at the apical surface of cornea epithelium. Moreover, in the immortalized corneal epithelial cells and conjunctival epithelial cells derived from the GDLD patient, the TJP1 and the occludin proteins were observed to be localized at the cell-to-cell borders, and the epithelial barrier function was found to be low.
The findings of this study indicate that in GDLD corneal epithelial cells, the tight junction is formed on the low level.
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Research Products
(9 results)
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[Journal Article] Establishment of a human corneal epithelial cell line lacking the functional TACSTD2 gene as an in vitro model for gelatinous drop-like dystrophy2013
Author(s)
Kitazawa K, Kawasaki S, Shinomiya K, Aoi K, Matsuda A, Funaki T, Yamasaki K, Nakatsukasa M, Ebihara N, Murakami A, Hamuro J, Kinoshita S
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Journal Title
Investigative Ophthalmology & Visual Science
Volume: 54(8)
Pages: 5701-5711
DOI
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