The localization of calcium-activated chloride channel and its contribution on related pathologic conditions
| Project/Area Number |
18592025
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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 |
Morphological basic dentistry
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| Research Institution | Fukuoka Dental College |
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Principal Investigator |
OKAMURA Kazuhiko Fukuoka Dental College, School of Dentistry, Associate Professor (00224056)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAZAKI Jun Fukuoka Dental College, School of Dentistry, Associate Professor (50230397)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥1,580,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥180,000)
Fiscal Year 2007: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2006: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | chloride channel / salivary gland / cancer cell / apoptosis / adhesion molecules / 局在 / イオン組成 / 顎下腺 / 導管 |
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| Research Abstract |
This project clarified how rat calcium-activated chloride channel-related (rCLCA) molecules distribute in the salivary gland (chiefly submandibular gland) both at physiological and pathologic states. rCLCA was localizad throughout the cytoplasmic organellae, namely rER, Golgi apparatus, early and late endosomes, et. Al. of the ductal sytem. Within the salivary ductal system, striated ducts and granular convoluted tubules showed the most intense localization of rCLCA, while the amount of rCLCA weakened in intercalated ducts and excretory ducts, and no rCLCA was detected in the serous and mucinous acinar cells. rCLCA molecules at the above ductal system colocalized with other chloride channel molecules such as CFTR. The function of rCLCA was analyzed with broad methodological approaches as molecular biology (the inhibition of mRNA procuction with siRNA), electro-physiology, pharmacology and biochemistry along with co-workers. Subsequently the interaction of rCLCA and CFTR and the influence of rCLCA on ion transport of salivary ductal system were partially clarified, and these products were published in international journals.
rCLCA expression was drastically depressed when the hyperplasia of acinar cells was induced by the isoproterenol administration; almost all rCLCA proteins disappeared except at the intercalated duct. Cell lines with stable rCLCAexpression showed decreased proliferative activity and increased apoptosis after the exposure of Staurosporine, compared with the same cell lines without rCLCAexpression.
Further exploration would be required to elucidate the other function of rCLCA both in physiologic and pathlogic states.
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Report
(3 results)
Research Products
(6 results)
