| Project/Area Number |
16K19390
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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 |
Cardiovascular medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
SOMA KATSURA 東京大学, 医学部附属病院, 特任臨床医 (90755696)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 肺高血圧 / 血管リモデリング / 右室リモデリング / マクロファージ / 炎症細胞 / 低酸素 / チアノーゼ性心疾患 / シャント性心疾患 / 好酸球 / 先天性シャント性心疾患 / 炎症シグナル |
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| Outline of Final Research Achievements |
Pulmonary arterial overflow associated with cardiac shunt induces pulmonary arterial remodeling, while its precise molecular mechanisms are yet to be determined. We established a novel murine pulmonary arterial overflow model. First, we resected left lung and induced redistribution of the cardiac output to the remaining right pulmonary artery, consecutively we exposed these mice to chronic hypoxia for 3 weeks, which elicited pulmonary arterial hypertension and right ventricular hypertrophy. Using this murine model, we performed histological study and Flow cytometry (FACS) analysis to track the population of lung inflammatory cells. FACS analysis showed an acute but transient accumulation of F4/80 positive, Ly6C low M2 macrophages in interstitial area. Depletion of these interstitial macrophages reduced pulmonary arterial remodeling. These results indicate that pharmacological inhibition of M2 macrophages can be a therapeutic target for the management of patients with PAH.
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