| Project/Area Number |
24591144
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
MIZUMO Shiro 金沢医科大学, 医学部, 准教授 (80397281)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIZAKI Takeshi 金沢医科大学, 医学部, 教授 (80151364)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | p53 / 血管内皮前駆細胞 / 喫煙 / 慢性閉塞性肺疾患 |
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| Outline of Final Research Achievements |
Patients, who have at least a 10 pack year history of tobacco exposure, were recruited from Department of Respiratory Medicine, Kanazawa Medical University and other institution. Genomic DNA were extracted from blood samples of the patients and gene polymorphisms of p53 codon 72 and MDM2 SNP309 were analyzed by PCR-RFLP. mRNA expressions of CD31, CD34 and vWF from blood, as a marker of circulating endothelial precursor cells, were measured by real-time RT-PCR. Both gene polymorphisms of p53 and MDM2 had influence on the development of emphysema. The mRNA expressions of CD31, CD34 and vWF were significantly decreased in the group of moderate COPD compared with the group of smoking control. These results indicate that decreased endothelial precursor cells in the blood from smoking patients had an impact on the pathogenesis of COPD.
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