| Project/Area Number |
23659818
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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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 |
SOTOZONO Chie 京都府立医科大学, 医学(系)研究科(研究院), 講師 (30216585)
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| Co-Investigator(Kenkyū-buntansha) |
OKUMURA Naoki 同志社大学, 生命医科学部, 助教 (10581499)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | アミノ酸 / 角膜 / 上皮細胞 / タイトジャンクション / 涙液 / ヒト角膜上皮細胞 / アルギニン / グルタミン酸 / グルタミン / アラニン / アスパラギン酸 |
|---|
| Research Abstract |
We examined the change of cell growth, wound healing, and barrier function of cultivated human corneal epithelial cells using specific culture medium including or deleting 1-23 amino acids. The proliferation of cultivated human corneal epithelial cells was inhibited by deleting Arg, Glu, Asn or Ala from the culture medium containing 23 amino acids (FULL medium). Arg deficit from culture medium also inhibited wound healing at the vitro wound-healing model. Transepithelial electrical resistance (TER) was high in FULL medium, and low in ZERO medium, indicating amino acids increase cell-cell adhesion. In an Arg deficit culture medium, TER dramatically decreased. In the Glu deficit culture medium and the Asn deficit culture medium, it also decreased.
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