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A study for the mechanism of progression of cell differentiation in osteoblast with ionizing radiation : Involvement of activation of signal transduction in cells.

Research Project

Project/Area Number 08877284
Research Category

Grant-in-Aid for Exploratory Research

Allocation TypeSingle-year Grants
Research Field 病態科学系歯学(含放射線系歯学)
Research InstitutionShowa University

Principal Investigator

HACHISU Reiko  Showa University, Dept.of Dentistry, Research Associate, 歯学部, 助手 (10164857)

Co-Investigator(Kenkyū-buntansha) YAMAMOTO Mika  Showa University, Dept.of Dentistry, Research Associate, 歯学部, 助手 (30276604)
HANAZAWA Tomomi  Showa University, Dept.of Dentistry, Research Associate, 歯学部, 助手 (20245872)
SANO Tsukasa  Showa University, Dept.of Dentistry, Assistant Professor, 歯学部, 講師 (40241038)
Project Period (FY) 1996 – 1997
Project Status Completed (Fiscal Year 1997)
Budget Amount *help
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1997: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1996: ¥1,500,000 (Direct Cost: ¥1,500,000)
KeywordsRadiation effect / Osteoblasts / Signal transduction / Cell differentiation
Research Abstract

We investigated a mechanism for progression of cell differentiation by free radicals formed with ionizing radiation. As the activation of signal transduction is possibly involved in the progression of cell differentiation with radiation, we used inhibitors of signal transduction to investigate the mechanism.
1.MC3T3-E1 cells, an osteoblast-like cell line, were irradiated with x-ray with 10 Gy on culture day3. Alkalinphosphatase (ALP) activity, one of differentiation marker, in the cells was increased from culture day 12.2.Addition of 50 mM Genistein, a tyrosine kinase inhibitor, slightly increased ALP specific activity in non-irradiated cells. On the other hand, in irradiated cells, increase of ALP specific activity after irradiation was inhibited by Genistein, showing comparable activity to non-irradiated control cells. Therefore, Genistein showed a possibility to inhibit the increase of ALP specific activity by the irradiation. 3.Fifty mM H-7, a non-specific serin/threonin kinase inhibitor, inhibited the increase of ALP specific activity after irradiation, while protein kinase C specific inhibitor of Calphostin C at 0.1 mM did not. 4.Neomycin, a phospholipase C inhibitor, also did not affect the increase of ALP specific activity in irradiated cells.
The results suggest a possibility that increase of ALP activity in MC3T3-E1 cells induced by the x-ray irradiation is consequence of activation of tyrosine kinase in signal transduction of the cells. Furthermore, activation of serin/threonin kinases such as protein kinase A other than protein kinase C is possibly incorporated for the increase of ALP activity after irradiation.

Report

(3 results)
  • 1997 Annual Research Report   Final Research Report Summary
  • 1996 Annual Research Report

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Published: 1996-04-01   Modified: 2016-04-21  

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