2018 Fiscal Year Final Research Report
Development of new treatment for short bowel syndrome using direct reprogramming
Project/Area Number |
16K11356
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pediatric surgery
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Research Institution | Nihon University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
古屋 武史 日本大学, 医学部, 研究医員 (20568539)
松本 太郎 日本大学, 医学部, 教授 (50366580)
越永 從道 日本大学, 医学部, 教授 (70205376)
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Project Period (FY) |
2016-10-21 – 2019-03-31
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Keywords | Direct reprogramming / 短腸症候群 |
Outline of Final Research Achievements |
We used the exosome derived from DFAT for gene delivery, because exosomes play an important role in intercellular communication, and it was reported that uptake into intestinal tissue can be seen by intraperitoneal administration, The DFAT-drived exosome can be confirmed as an endoplasmic reticulum of 100-200 nm by electron microscopy, and CD69, which is a marker of exosome, was confirmed by western blotting. To produce the model mice, 5% DSS was administered orally for 1 week, The involvement of adipocytes on the site of intestinal injury was examined histologically. Under the above conditions, the adipocytes were not involve for intestinal regeneration.
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Free Research Field |
細胞再生
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Academic Significance and Societal Importance of the Research Achievements |
脂肪は皮下だけでなく、臓器の周囲にも多く存在する。脂肪運命の追跡可能なマウスを用いて、様々な疾患モデルマウスにおいて周囲脂肪組織の脂肪細胞の挙動を確認することは、それらの疾患と脂肪とのかかわりを解明することとなり、疾患の発症予防、新規治療などにつながる。 本研究においてはモデルマウスの作成に難渋したが、今後は腸炎モデル以外にも、肥満と腫瘍のかかわりが指摘されている乳癌などにおいて、脂肪細胞の挙動を同様の手法を用いることで確認し、発症予防や新たな治療戦略の可能性を探る。
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