| Project/Area Number |
14370656
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | University of Tsukuba |
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Principal Investigator |
YOSHIDA Hiroshi University of Tsukuba, Graduate School of Comprehensive Human Sciences, Professor, 大学院・人間総合科学研究科, 教授 (80014330)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Masayuki University of Tsukuba, Graduate School of Comprehensive Human Sciences, Professor, 大学院・人間総合科学研究科, 教授 (50166823)
ISHII Tetsuro University of Tsukuba, Graduate School of Comprehensive Human Sciences, Professor, 大学院・人間総合科学研究科, 教授 (20111370)
YANAGAWA Toru University of Tsukuba, Graduate School of Comprehensive Human Sciences, Assistant professor, 大学院・人間総合科学研究科, 講師 (10312852)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥13,600,000 (Direct Cost: ¥13,600,000)
Fiscal Year 2004: ¥4,500,000 (Direct Cost: ¥4,500,000)
Fiscal Year 2003: ¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 2002: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | Peroxiredoxin / knockout mouse / gene trapping / GATA-1 / MSP23 |
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| Research Abstract |
Prx I deficient mouse was established by gene trapping method. Embryonic stem (ES) cells with a retroviral gene trap vector inserted into the Prx I locus (Omni bank no.OST422296) were transferred to a foster mother to generate chimeric animals (Lexicon Genetics Inc.). The genetic background was uniformized to C57BL/6 by back cross. B16 murine melanoma cells (1x10^5 cells/body) were inoculated into the mouse foot pad of three groups (wild-type, heterozygous, and homozygous Prx I deficient mouse) and lymph node metastasis and lung metastasis were observed. When genetic background was C57/129Sv, lymph node and lung metastasis were reduced by Prx I loss. However, after 5 generation back cross and uniformized C57BL/6 genetic background, there was no significant difference in lymph node and lung metastasis between wild-type and Prx I homozygous deficient mice. When another cell line (LLC cell, derived form lung cancer : 3x10^6 cells/body) was inoculated in these groups, there was no difference. By using Matrigel as a matrix of tumor growth, we inoculated the mixture of B16 cells (1x105 cells /body) and the gel into subcutaneous and investigated the vascularization, but there was no significant difference. On the other hand we investigated the stress response of A170 oxidative stress, which is regulated by same transcription factor Nrf2 as Prx I to analyze how oxidative stress protein was induce by oxidative stress. And we also investigated GATA-1 transgenic mouse, because Prx I and GATA-1 were both related with red blood cell abnormality.
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