| Project/Area Number |
16590743
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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 |
Respiratory organ internal medicine
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| Research Institution | University of Fukui |
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Principal Investigator |
ISHIZAKI Takeshi University of Fukui, Faculty of Medicine, Professor, 医学部, 教授 (80151364)
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| Co-Investigator(Kenkyū-buntansha) |
AMESHIMA Shingo University of Fukui, University of Fukui Hospital, Lecturer, 医学部附属病院, 講師 (60262614)
DEMURA Yoshiki University of Fukui, University of Fukui Hospital, Assistant Professor, 医学部附属病院, 助手 (60313764)
MIZUNO Shirou University of Fukui, Faculty of Medical Sciences, Assistant Professor, 医学部, 助手 (80397281)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | hypoxia / NO donor / PGI2 analogue / human pulmonary arterial cell / p21 / p27 / p53 / p53 knock-out mouse / CDKインヒビター / PGI_2 |
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| Research Abstract |
1) To assess the suppressive effects of NO donor and PGI2 analogue on proliferation of the human cultured pulmonary arterial smooth muscle cells (HPASMC) under the circumstance of 2% hypoxic oxygen.
NO donor and PGI2 suppressed the intake of BrdU and ceased cell cycle at G0/1 phase in HPASMC. Concordantly, NO donor induced p21 mRNA, and augmented the protein expression of p21 and p53. PGI2 analogue augmented the protein expression of p27.
2) Tb compare the thickness of pulmonary arterial wall of p53 knock-out mouse with wild-type mouse treated in the circumstance of 2% hypoxic oxygen for 8 weeks.
The thickness of pulmonary arterial wall of p53 knock-out mouse was greater than that of wild-type mouse.
These results were suggesting that suppression of p53, p21 and p27 are taking a role in the progression of hypoxia induced proliferation of HPASMC, and endogenous NO and PGI2 are having anti-proliferative effect on HPASMC via maintaining the activity of p53, p21 and p27.
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