| Project/Area Number |
17K09591
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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 |
Cardiovascular medicine
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| Research Institution | Kyushu University |
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Principal Investigator |
Kohtaro Abe 九州大学, 大学病院, 助教 (20588107)
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| Co-Investigator(Kenkyū-buntansha) |
筒井 裕之 九州大学, 医学研究院, 教授 (70264017)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 肺高血圧症 / 炎症 / 血行動態ストレス / 肺高血圧 / 閉塞性病変 / 閉塞性肺血管病変 |
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| Outline of Final Research Achievements |
The purpose of this study was to analyze mtDNA and TLR9 activities in the development and maintenance of obstructive lesions in pulmonary hypertension. When monocrotaline was administered to male SD rats, plasma mtDNA markers and lung cleaved TLR9 protein were time-dependently increased after days 1,3,7,14 after monocrotaline injection. In parallel with TLR9 activation, inflammatory cell infiltration around pulmonary small blood vessels and increase in IL-6 mRNA with time were observed. When non-selective TLR9 inhibitor chloroquine was administered for 3 days from day 14, significant reductions of IL-6 and macrophages was observed, suggesting that mtDNA and TLR9 may be deeply involved in the inflammatory mechanism of pulmonary hypertension.
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| Academic Significance and Societal Importance of the Research Achievements |
肺高血圧症の病態進展に深くかかわる炎症誘導機構の解明は、難治性疾患の肺高血圧症の新規治療法につながる可能性がある。
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