| Project/Area Number |
26860620
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | University of Occupational and Environmental Health, Japan |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 肺高血圧 / 一酸化窒素 / Nitric oxide / Pulmonary Hypertension / Bone marrow / Nitric oxide synthase / 低酸素性肺高血圧 / 一酸化窒素合成酵素 / NOS |
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| Outline of Final Research Achievements |
The role of nitric oxide synthases (NOSs) in the development of pulmonary hypertension (PH) has been examined in pharmacological studies with non-selective NOSs inhibitors. However, due to the non-specificity of the NOSs inhibitors, the authentic role of NOSs in PH still remains to be clarified. We show here that hypoxia-induced PH was markedly deteriorated in triply
n/i/eNOSs-/- genotype and, to a lesser extent, in eNOS-/- genotype, but not in nNOS-/- or
iNOS-/- genotype, as compared with WT genotype. In addition, transplantation of triply NOSs-/- bone marrow results in the exacerbation of hypoxia-induced PH in mice, demonstrating the protective role of myelocytic NOSs in the pathogenesis of PH. Our findings provide novel insights into the cellular and molecular bases of PH.
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