| Project/Area Number |
26461457
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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 |
Collagenous pathology/Allergology
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| Research Institution | Tohoku University |
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Principal Investigator |
Shirota Yuko 東北大学, 大学病院, 助教 (20455819)
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| Co-Investigator(Kenkyū-buntansha) |
石井 智徳 東北大学, 大学病院, 特任教授 (10282138)
藤井 博司 東北大学, 医学系研究科, 准教授 (30531321)
藤原 亨 東北大学, 大学病院, 講師 (60333796)
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 肺動脈性肺高血圧症 / 転写因子GATA2 / 肺高血圧 / 単球 / マクロファージ / 転写因子ＧＡＴＡ２ / 骨髄由来免疫抑制細胞 / Toll様受容体 |
|---|
| Outline of Final Research Achievements |
We investigated the role of transcription factor GATA-2 and Myeloid derived suppressor cell (MDSC) and macrophage in pulmonary arterial hypertension (PAH). 1) In human pulmonary tissues, there are more GATA2+CD68+ macrophage cell infiltrated in PAH compared to healthy control. 2) Peripheral MDSC subsets were significantly increased in human PAH compared to controls. 3) We established GATA2 conditional knock out mice, and those mice and control mice were induced PAH in hypoxia condition. Right ventricle hypertrophies were highly occurred in controls compared to GATA2-KO. The pulmonary arteries remodeling was equally occurred in both group. On the other hand, there were more inflammatory cells infiltrated in GATA-2 KO. In human PAH, GATA2 expression might be upregulated, however, we could not have definite tendency in inducing PAH in GATA2-KO model. We would like to investigate additional experiments.
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