Elucidation of mechanism on dentin hypersensitivity; cell response by hypertonic stress.
Project/Area Number |
24592876
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Conservative dentistry
|
Research Institution | Kagoshima University |
Principal Investigator |
MASAYUKI Tokuda 鹿児島大学, 医歯(薬)学総合研究科, 准教授 (20253891)
|
Co-Investigator(Kenkyū-buntansha) |
MORIMOTO Yoko 鹿児島大学, 医学部・歯学部附属病院, 助教 (30437967)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 象牙質知覚過敏症 / 象牙芽細胞 / スクロース / 高浸透圧 / 細胞死 / 分裂促進因子活性化タンパク質キナーゼ / キシリトール / TRPV1 / AQP2 / 浸透圧 / 細胞内転写因子 |
Outline of Final Research Achievements |
Osmotic stress is one cause of dental pain due to caries or dentin hypersensitivity. The mechanism of osmotic-induced dental pain is not completely understood. The purpose of this study was to examine the responses of odontoblasts under sucrose-induced hyperosmotic stress. Cell viability decreased over 700 mOsm for 3 h cell culture. The shapes of cells and nuclei became irregular and vacuolar under hyperosmotic stress. The expression of cleaved caspase-3 was increased after treatment with hyperosmotic stress. Flow cytometry analysis detected no annexin V-positive cells, indicating apoptosis. Three MAPKs phosphorylation were induced by hyperosmotic stress. Inhibitors of three MAPKs inhibited the hyperosmotic stress-induced decline in cell cultures at 500 and 700 mOsm. Hyperosmotic stress induces cell death of OLCs with sucrose through a MAPK pathway.
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Report
(4 results)
Research Products
(4 results)