2001 Fiscal Year Final Research Report Summary
The role of intercellular communication in osteoblastic differentiation
| Project/Area Number |
12672001
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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 |
矯正・小児・社会系歯学
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
MIURA Kazuo Hiroshima University, Faculty of Dentistry, Assistant Professor, 歯学部, 助教授 (30034185)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Junji Hiroshima University, Faculty of Dentistry, Research Associate, 歯学部, 助手 (90263714)
OKADA Mitsugi Hiroshima University, Faculty of Dentistry, Research Associate, 歯学部, 助手 (10233347)
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| Project Period (FY) |
2000 – 2001
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| Keywords | Intercellular communication / osteoblast / differentiation / connexin43 / phenytoin / real^-time RT-PCR / dominant negative / transfect |
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| Research Abstract |
The hypothesis of this study is the gap junctional intercellular communication modulates cell differentiation in osteoblast. To test the hypothesis, we carried out two projects as follows.
Project 1
We established deletion mutant cDNA of connexin43 that mediates gap junctional intercellular communication and transfected into MC3T3-E1 cells, Eventually, we got two stable transfectants. These cells expressed dominant negative of deletion mutated connexin43 and were inhibited intercellular communication almost half of vector control. Furthermore, the expression of differentiation markers was inhibited remarkably. It means the differentiation in osteoblast was mediated in part by gap junctional intercellular communication.
Project 2
Although phenytoin is often used as anticonvulsant drag, it caused side effect. We test whether phenytoin effects on intercellular communication in osteoblast or not. Phenytoin promoted gap junctional intercellular communication in MCT3T3-E1 to 1.6-hold of control, further cell differentiation was increased almost 9 times higher than control. It suggests phenytoin induces differentiation in osteoblast via modulating intercellular communication.
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