The regulation of human organ structure by position fate genes
| Project/Area Number |
18K19535
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Review Section |
Medium-sized Section 53:Organ-based internal medicine and related fields
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
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| Project Period (FY) |
2018-06-29 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2019: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2018: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
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| Keywords | 位置運命決定因子 / 病変好発部位 / 疾患感受性 / 疾患好発部位 / オルガノイド |
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| Outline of Final Research Achievements |
I established human colonic organoids generated from the left rectum and the right ascending colon of colectomy specimens in the same patient, respectively. After evaluating cell function such as cell proliferation, stem cell fraction, inflammatory stimulation response and inflammatory stimulation tolerance, I detected the suppression of cell proliferation in the organoid derived from rectum. I also extracted the gene which was specifically expressed in each organdies. Moreover, I confirmed that the expression was stored in human by the analysis of the operative specimen. Furthermore, I discovered that these genes affect on a cell function as well as a position decision function.
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| Academic Significance and Societal Importance of the Research Achievements |
現在様々な疾患に関して病態解明が行われているが、好発部位を主眼とした病態解明は殆どない。特にIBDは炎症を主眼とした免疫制御破綻の観点からの病態解明が多くされてきており、実臨床においても免疫抑制療法が主流である。しかし、免疫抑制療法のみでは再燃が多く完治しないことが問題となり粘膜再生が重要視されるようになった。粘膜が再生すると上皮細胞による消化管バリアー機能が作動し再燃が抑制されることが提唱され、近年腸管上皮細胞の機能が注目されている。逆に言えば、ある特定の部位の上皮が破綻すればその部位が病変部になることを示しており、IBD好発部位における上皮破綻機能の解明が疾患克服に繋がると期待される。
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Report
(3 results)
Research Products
(18 results)
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[Presentation] Synergy of Notch signalling and TNF-α in the inflamed intestinal epithelia of IBD patients leads to up-regulation of UBD, a ubiquitin-like protein.2019
Author(s)
Kawamoto A, Nagata S, Anzai S, Takahashi J, Kawai M, Hama M, Nogawa D, Yamamoto K, Kuno R, Suzuki K, Shimizu H, Hiraguri Y, Yui S, Oshima S, Tsuchiya K, Nakamura T, Ohtsuka K, Kitagawa M, Okamoto R, Watanabe M
Organizer
ECCO2019
Related Report
Int'l Joint Research
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