| Co-Investigator(Kenkyū-buntansha) |
橋本 真一 和歌山県立医科大学, 先端医学研究所, 教授 (00313099)
上羽 悟史 東京理科大学, 研究推進機構生命医科学研究所, 准教授 (00447385)
伊藤 利洋 奈良県立医科大学, 医学部, 教授 (00595712)
七野 成之 東京理科大学, 研究推進機構生命医科学研究所, 助教 (70822435)
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| Budget Amount *help |
¥320,060,000 (Direct Cost: ¥246,200,000、Indirect Cost: ¥73,860,000)
Fiscal Year 2021: ¥61,360,000 (Direct Cost: ¥47,200,000、Indirect Cost: ¥14,160,000)
Fiscal Year 2020: ¥61,360,000 (Direct Cost: ¥47,200,000、Indirect Cost: ¥14,160,000)
Fiscal Year 2019: ¥61,360,000 (Direct Cost: ¥47,200,000、Indirect Cost: ¥14,160,000)
Fiscal Year 2018: ¥61,360,000 (Direct Cost: ¥47,200,000、Indirect Cost: ¥14,160,000)
Fiscal Year 2017: ¥74,620,000 (Direct Cost: ¥57,400,000、Indirect Cost: ¥17,220,000)
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| Outline of Final Research Achievements |
The objective of this project was to identify new preventive targets of pulmonary fibrosis by identifying molecules and cell subsets involved in the transition and regulation of the "inflammatory cell society," which is composed of the interaction of various cell types. We developed a novel scRNA-seq analysis method, TAS-Seq, which is much more sensitive and accurate than existing technologies, and identified C1q as a specific molecule for interstitial macrophages, which increase with the progression of silica-induced pulmonary fibrosis, and found that C1q directly affects fibroblasts and alveolar epithelial cells to promote fibrosis. Furthermore, we have constructed a temporal network model of the transition of inflammatory cell society based on temporal scRNA-seq data, and have identified and are validating the transition of hub cells and multiple secreting factors derived from them.
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