2012 Fiscal Year Final Research Report
Role of tight junction (claudin) in the regulation of endocochlear potential
| Project/Area Number |
22590217
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Osaka Medical College |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
山路 純子 (田代 純子) 大阪医科大学, 医学部, 講師 (40340559)
白岩 有桂 大阪医科大学, 医学部, 助教 (20596605)
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| Project Period (FY) |
2010 – 2012
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| Keywords | 内リンパ腔電位 / クローディン / タイト結合 / 血管条辺縁細胞 / Ca2+濃度 |
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| Research Abstract |
It had been reported that mutatios in the gene encoding claudin-14 cause deafness and nephrolithiasis. In this experiment, we made the claudin-14 knockout mice to examine the functional role of tight junctions in the endolyphatic surface cells. The obtained experimental results were as follows; 1) endocochlear potential (EP) in the endolymph in knockout mice was lower than that in wild type mice. In the preset, we are trying to measure the H+, K+, Na+,Ca2+ concentrations in endolymph. All above experimental results will be published in the next year.
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[Journal Article] Transgene number-dependent, gene expression rate-independent rejection of Dd-, Kd-, or DdKd-transgened mouse skin or tumor cells from C57BL/6(DbKb)mice.2011
Author(s)
Inoue Y, Tashiro-Yamaji J, Hayashi M, Kiyonari H, Shimizu T, Ibata M, Yamana H, Kubota T, Tanigawa N, Yoshida R
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Journal Title
Microbiol Immunol
Volume: 55
Pages: 446-453
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