| Project/Area Number |
24580433
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Basic veterinary science/Basic zootechnical science
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| Research Institution | Nihon University |
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Principal Investigator |
SUGIYA Hiroshi 日本大学, 生物資源科学部, 教授 (20050114)
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| Co-Investigator(Renkei-kenkyūsha) |
NARITA Takanori 日本大学, 生物資源科学部, 専任講師 (70453884)
OKABAYASHI Ken 日本大学, 生物資源科学部, 専任講師 (20409072)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 生理・細胞機能 / 耳下腺 / 開口分泌 / cAMP / Rho / Rhoキナーゼ / アクチン / 耳下腺腺房細胞 / RhoA / 開口放出 |
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| Outline of Final Research Achievements |
In rat parotid acinar cells, stimulation of β-adrenergic receptors provokes an increase in intracellular cAMP level, resulting in amylase release. We studied involvement of Rho family, a member of Ras superfamily proteins, in the amylase release. A protein band ADP-ribosylated by Clostridium botulinum C3 (C3), an inhibitor of the function via ADP-ribosylation of Rho, was detected in the cells. The same protein band was cross-reacted with anti-RhoA antibody. RhoA was activated by the β-agonist isoproterenol (IPR). C3 blocked the cAMP-induced amylase release in permeabilized cells. The IPR-induced RhoA activation was inhibited by a PKA inhibitor. The Rho kinase inhibitor Y-27632 partially inhibited the IPR-induced and dibutyryl cAMP-induced amylase release. In the cells treated with Y-27632, IPR-induced distribution of cortical F-actin was disturbed. These results suggest that RhoA/ROCK signaling is involved in cAMP-dependent amylase release in rat parotid acinar cells.
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