| Project/Area Number |
09680826
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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 |
Laboratory animal science
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| Research Institution | University of Tsukuba |
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Principal Investigator |
FUKAMIZU Akiyoshi (1998) Institute of Applied Biochemistry, University of Tsukuba, 応用生物化学系, 助教授 (60199172)
杉山 文博 (1997) 筑波大学, 基礎医学系, 講師 (90226481)
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| Co-Investigator(Kenkyū-buntansha) |
HORIGUCHI Hisashi Ibaraki Prefectural University of Health Sciences, 助手 (30238795)
YAGAMI Ken-ichi Institute of Basic Medical Sciences, University of Tsukuba, 基礎医学系, 教授 (40166476)
深水 昭吉 筑波大学, 応用生物化学, 助教授 (60199172)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Angiotensinogen / knockout / Renin-angiotensin system / Hydronephersis / Blood-brain barrier / アンギオテンシンII / 高血圧 / トランスジェニックマウス / 1型受容対 / 2型受容対 / アポトーシス / アンギオテンシノーゲン遺伝子欠損マウス / 腎 / 実験動物 |
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| Research Abstract |
We previously developed hypotensive mice by gene-targeting technique to understand the function of angiotensinogen gene. The angiotensinogen-deficient (AgtKO) mice were maintained with mixed C57BL/6J, CBA, and ICR hybrid genetic background. Therefore development of AgtKO mice with homogeneous genetic background is needed. 1) We developed AgtKO with genetic background of C57BL/6J (C57BL/6J-AgtKO) by speedy backcrossing through in virtro fertilization, using pre-pubertal superovulation. 2) We demonstrated that C57BL/6J-AgtKO mice die before weaning. 3) We indicated that mortality in C57BL/6J-AgtKO can be reduced by hypodermic saline injection in the 7 days following birth and that C57BL/6J-AgtKO are developed hydronephrosis by day 14. 4) The apoptotic induction is involved in the development of hydronephrosis on C57BL/6J-AgtKO. 5) We also demonstrated that the hydronephrosis is prevented by genetic rescue of the angiotensinogen gene. 6) Furthermore we indicated that the Agt gene are required for functional maintenance of blood-brain barrier.
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